Practice Guidelines for Family

Nurse Practitioners
FOURTH EDITION

Karen Fenstermacher, MS, RN, FNP-BC

Family Nurse Practitioner, Mercy Primary Care, Carthage, Missouri

Barbara Toni Hudson, MSN, RN, FNP-BC

Family Nurse Practitioner, Ash Grove Family Care Clinic, Citizens Memorial Hospital, Ash Grove,
Missouri

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Table of Contents
Cover image
Title page
Inside Front Cover
Copyright
Reviewers
Preface
Acknowledgments

1. History and Physical Examination

1. Adult assessment
Focused examinations
2. Pediatric assessment
Guidelines for comprehensive pediatric assessment
3. Geriatric assessment
Introduction
Comprehensive geriatric assessment
Assessing cognitive and emotional status
Functional assessment
Falls
4. Laboratory and diagnostic pearls
General
Hematology (CBC)
Urine
Liver
Chemistries
Miscellaneous
Lab tests for arthralgias
Radiology pointers

2. Common Conditions
5. Skin conditions
Disorders causing inflammation
Disorders caused by infection
Disorders caused by viral infections

3
 Disorders caused by fungal infection
Disorders of pigmentation
Skin lesions
Wound care
Incision and drainage (I & D) of an abscess
Things that bite and sting
6. Respiratory conditions
7. Eye, ear, nose, and throat conditions
Ocular complaints
8. Cardiovascular conditions
9. Peripheral vascular and hematologic conditions
Chronic peripheral vascular diseases
Chronic wound management
Anemia
10. Abdominal conditions
Upper abdominal problems
Lower abdominal problems
Hepatitis illnesses
Bariatric surgery
11. Gynecologic conditions
Screenings and pap smears
Contraception
Conditions related to menstruation
Breast conditions
Gynecologic conditions
Sexually transmitted diseases
12. Common urinary tract conditions
Common urinary tract disorders in men and women
Common genitourinary tract disorders in men
13. Neurologic conditions
14. Musculoskeletal conditions
History
Location-specific musculoskeletal disorders
General musculoskeletal disorders
15. Pain
Assessment of pain
Therapies for pain
16. Endocrine conditions
Thyroid disorders

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 Adrenal disorders
Diabetes mellitus
17. Pediatric conditions
Upper respiratory tract disorders
Lower respiratory tract disorders
Abdominal disorders
Genitourinary tract disorders
Musculoskeletal system disorders
Hematopoietic system disorders
Gynecological disorders
Neurological disorders
Cardiac disorders
18. Psychiatric conditions
Initial office visit
Mood disorders
Cognitive impairment
Food sources for selected nutrients
Index
Inside Back Cover
Color Plates

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Inside front cover
UNIT I History and physical examination, 1

1 Adult Assessment, 1
2 Pediatric Assessment, 25
3 Geriatric Assessment, 48
4 Laboratory and Diagnostic Pearls, 66

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UNIT II Common conditions, 77
5 Skin Conditions, 77
6 Respiratory Conditions, 123
7 Eye, Ear, Nose, and Throat Conditions, 140
8 Cardiovascular Conditions, 155
9 Peripheral Vascular and Hematologic Conditions, 191
10 Abdominal Conditions, 220
11 Gynecologic Conditions, 253
12 Common Urinary Tract Conditions, 287
13 Neurologic Conditions, 305
14 Musculoskeletal Conditions, 319
15 Pain, 352
16 Endocrine Conditions, 359
17 Pediatric Conditions, 395
18 Psychiatric Conditions, 424
Appendix A Food Sources for Selected Nutrients, 441

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Copyright

3251 Riverport Lane

St. Louis, Missouri 63043

PRACTICE GUIDELINES FOR FAMILY NURSE PRACTITIONERS, FOURTH EDITION

ISBN: 978-0-323-29080-7

Copyright © 2016, 2014, 2004 by Elsevier

All rights reserved. No part of this publication may be reproduced or transmitted in any form or
by any means, electronic or mechanical, including photocopying, recording, or any information
storage and retrieval system, without permission in writing from the publisher. Details on how
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This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).

Notices
Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our understanding, changes in research methods, professional practices,
or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described
herein. In using such information or methods they should be mindful of their own safety and
the safety of others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to
check the most current information provided (i) on procedures featured or (ii) by the
manufacturer of each product to be administered, to verify the recommended dose or
formula, the method and duration of administration, and contraindications. It is the

8
 responsibility of practitioners, relying on their own experience and knowledge of their
patients, to make diagnoses, to determine dosages and the best treatment for each individual
patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or
editors, assume any liability for any injury and/or damage to persons or property as a matter
of products liability, negligence or otherwise, or from any use or operation of any methods,
products, instructions, or ideas contained in the material herein.

Previous editions copyrighted 2014 (revised), 2004, 2000, 1997

Library of Congress Cataloging-in-Publication Data Fenstermacher, Karen, author.

  Practice guidelines for family nurse practitioners/Karen Fenstermacher, Barbara Toni
Hudson.—.
  p. ; cm.
  Includes bibliographical references and index.
  ISBN 978-0-323-29080-7 (spiral bound: alk. Paper) I. Hudson, Barbara Toni, author. II. Title.
  [DNLM: 1. Nurse Practitioners. 2. Family Nursing—methods. WY 128]
 RT120.F34
610.73—dc23 2013020571

Executive Content Strategist: Lee Henderson Associate Content Development Specialist: Samantha
Dalton Publishing Services Manager: Julie Eddy Project Manager: Jan Waters
Designer: Brian Salisbury

Printed in the United States of America

Last digit is the print number: 9 8 7 6 5 4 3 2 1

9
Reviewers
Sameeya Ahmed-Winston, RN, MSN, CPNP, CPHON Pediatric Nurse Practitioner, Children’s
National Medical Center, Washington, D.C.
Margaret-Ann Carno, PhD, MBA, RN, CPNP, D, ABSM, FAAN Associate Professor of Clinical
Nursing and Pediatrics, School of Nursing, University of Rochester, Rochester, New York Robin
Webb Corbett, PhD, FNP-C, RNC Associate Professor, East Carolina University College of
Nursing, Greenville, North Carolina Laura Crisanti, MSN, CCRN, CPNP-PC/AC Pediatric
Nurse Practitioner, Ann & Robert H. Lurie Children’s Hospital of Chicago, Chicago, Illinois
William Mark Enlow, DNP, ACNP, CRNA, DCC Assistant Professor, Columbia University
School of Nursing, New York, New York Mary A. Blaszko Helming, PhD, APRN, FNP-BC,
AHN-BC Professor of Nursing, Quinnipiac University School of Nursing, Hamden, Connecticut
Kathleen Sanders Jordan, DNP, MS, RN, FNP-BC, SANE-P Nurse Practitioner/Lecturer, School
of Nursing, Mid-Atlantic Emergency Medical Associates and the University of North Carolina at
Charlotte, Charlotte, North Carolina Kari Ksar, RN, MS, CPNP Pediatric Nurse Practitioner,
Lucile Packard Children’s Hospital, Palo Alto, California Suzanne Kujawa, RNC, MSN, CPNP-
PC Pediatric Nurse Practitioner, Ann & Robert H. Lurie Children’s Hospital of Chicago, Chicago,
Illinois Kelley S. Madick, MSN, CNP, DNPc Faculty, Kaplan University, Davenport, Iowa
Jessica A. Pech, APN, MSN, CPNP Pediatric Nurse Practitioner, Ann & Robert H. Lurie
Children’s Hospital of Chicago, Chicago, Illinois Caroline A. Rich, RN, MSN, CPNP-AC/PC
Pediatric Nurse Practitioner Pediatric Neurology, Helen DeVos Children’s Hospital, Grand
Rapids, Michigan Jill Harpst Rodgers, DNP, CRNP, MSN, RN Assistant Professor of Graduate
Nursing, Carlow University, Pittsburgh, Pennsylvania Dr. Michelle Taylor Skipper, DNP, FNP-
BC Clinical Associate Professor, East Carolina University College of Nursing, Greenville, North
Carolina Laura Steadman, Ed.D, CRNP, MSN, RN Assistant Professor, University of Alabama at
Birmingham, Birmingham, Alabama

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Preface
Karen Fenstermacher, Barbara Toni Hudson Practice Guidelines for Family Nurse Practitioners is a
quick reference book for practicing and student nurse practitioners in a variety of disciplines.
Although not intended as a textbook, it is an excellent resource, providing protocols for
treatment options for patients of varied ages in varied settings.
For ease of use, Unit I contains chapters about complete and detailed histories and physical
examinations of adult, pediatric, and geriatric patients. Specialized physical examinations are
included (e.g., sports). Chapters are written in an easy-to-read and accessible format according to
body systems. Common diseases are covered, including signs and symptoms, diagnostic
methods, drug therapies, and treatment and adjunctive therapies. Some conditions (e.g.,
cognitive impairment, anemia, and diabetes) have been expanded. Updated national standard
guidelines are used where available (e.g., asthma, diabetes, lipid treatment, Pap smears).
Special chapters include geriatric evaluation, pediatrics, and psychiatric conditions. There is
also a section on the care of wounds resulting from vascular disease or peripheral pressure. The
Appendix provides information about dietary sources of different nutrients. Pain management
guidelines have been expanded.

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Acknowledgments
My thanks first to God, without whose help I would not be where I am now. Also, thank you to
Tammy (the nurse I have worked with for 20 years!) and Karrie; you both make my job much
easier and I wouldn’t want to do it without you.
Karen

My thanks go to my family, David and Cody, for all their support, encouragement, and
understanding for all the lost time. I cannot forget my faithful friends, Kim, Lynda, and Ann for
their hours of help with reading and re-reading the chapters.
Toni

We are (and have been) very blessed to have many collegial relationships with physicians,
nurse practitioners, and physician assistants who we work with, consult with, and refer to—too
many to name individually, but we thank you all! We also are blessed to have the trust of the
patients we see, and we have learned much from them.
Karen and Toni

We also want to thank the people at Elsevier for all their help; our book would not be what it is
without their input.

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UNIT I

History and Physical Examination

OUTLINE

1. Adult assessment
2. Pediatric assessment
3. Geriatric assessment
4. Laboratory and diagnostic pearls

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CHAPTER 1

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Adult assessment
Guideline for integrated, comprehensive physical examination*

History

I. Biographic information (e.g., “facesheet information”)

II. Chief complaint (CC)

A. State in the patient’s own words

B. Note if the patient’s actions agree with or contradict the stated CC
III. History of the present illness (HPI)

A. Try to present a clear account of the patient’s CC, including what

treatments have been tried before (what worked and what did not) B.
Question the patient regarding the following:
1. Onset (e.g., when, where)
2. Characteristics (e.g., description of the quality of discomfort, radiation,
associated symptoms such as N/V) 3. Course (e.g., length of the event,
alleviating or aggravating factors) 4. What does the patient think is
wrong?
C. Also note pertinent negative responses (e.g., absence of cough or
fever)
IV. Past medical history (PMH)

A. This tells the nurse practitioner when to be more concerned (e.g.,

someone with an essentially negative PMH is not as worrisome as a
patient with heart disease or an underlying chronic illness) B. Question
the patient regarding significant childhood and adult illnesses,
surgeries, and hospitalizations, including emergency department visits
C. Ask about current medications and treatments, including OTC
preparations, OCs, inhalers, eye drops, herbal supplements or
vitamins, and customs (e.g., home remedies, cultural treatments) D.
Ask about the immunization status, including influenza,
pneumococcal vaccines (Pneumovax 23 and Prevnar 13), shingles
vaccine, and TB test E. Ask whether the patient has reactions (e.g.,

15
 allergies, sensitivities) to any medicine and what occurs when the
medicine is taken (common side effects such as nausea are often
perceived as an allergy) F. Ask about street drug, alcohol, and tobacco
use (specific types, amounts, and routes)
V. Family history (FH)

A. FH is important for the identification of risk factors; gather

information about grandparents, parents, and siblings B. Focus on
cardiovascular disease, DM, cancer, PVD, seizure disorders, asthma,
and psychiatric disorders C. The phrase “significant FH” indicates that
several family members from different generations have had a specific
disease
VI. Psychosocial history

A. Living situation, including significant other in life

B. Dietary and rest patterns
C. Types and frequency of exercise
D. Occupation
E. Spiritual assessment
1. Faith or beliefs
2. Importance and influence in the patient’s life
3. Involvement in a religious/spiritual community and is this a support to
the patient
VII. Review of systems (ROS): offers the chance to systematically investigate various body
systems to obtain any additional information that would be helpful in arriving at an accurate
diagnosis VIII. Recording the history: record historical data in the above sequence, remembering
to include pertinent positive and negative responses and pertinent past laboratory data.

Physical examination

I. General appearance (e.g., grooming and dressing, facial expressions, symmetry of movement)
and skin color and turgor

A. Appears acutely ill

B. Signs of dehydration (e.g., dry mucous membranes, tachycardia,
dizziness) C. Cyanosis or pallor
D. SOB or use of accessory muscles to breathe

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 E. Drooling (epiglottitis; see Chapter 17)
II. Vital signs: temperature, pulse, respiration, BP (including postural VS with dizziness or
syncope), weight, height, and BMI

A. Postural VS changes: initially determine the VS with the patient lying

quietly; next have the patient sit (and then stand, if indicated) and
within 2 to 5 minutes of position change(s), recheck the VS. With
postural changes, one or more of the following will happen:
1. ≥20 mmHg drop in systolic BP
2. ≥10 mmHg drop in diastolic BP
3. Patient becomes symptomatic (e.g., dizzy)
B. A low diastolic BP (<65 mmHg) implies decreased peripheral
resistance or aortic valve regurgitation (which is significant, even if the
heart sounds are not loud)
III. Inspect the skin

A. Fingernail clubbing
B. Suspicious or unusual lesions
IV. Head, ears, eyes, nose, and throat (HEENT)

A. Inspect the face and head

B. Palpate the scalp, temporal area for pulsation, and masseter muscles
(have the patient clench his or her teeth) C. Eyes
1. Check for the best visual acuity: right eye, left eye, and both eyes (note
with/without corrective lenses)
a) distance (e.g., Snellen chart)
b) newsprint (document how far away it is held to read, e.g., 6 inches) c)
counting fingers
d) hand motion
e) light perception
f) no light perception
2. Check for pupil reactivity: shine light first in the unaffected eye (both
pupils should constrict) and then in the affected eye; if pupils dilate,
the optic nerve in the affected eye is not working (see Marcus Gunn
pupil, Table 1-3) 3. Pressure: gently press on closed eyes for symmetry

17
4. Peripheral visual fields: sit/stand at eye level directly in front of the
patient to check peripheral field vision 5. Alignment
a) have the patient look straight ahead toward the light—the light
reflection should be symmetrical b) test extraocular muscles (EOMs)
c) nystagmus
6. External: observe lid symmetry
7. Anterior: examine the conjunctiva, sclera, and cornea
a) red eye or drainage
8. Perform ophthalmoscopy, if possible; refer if dilated examination is
needed
D. Ears
1. Palpate the auricle and tragus
2. Perform otoscopy (Figure 1-1)
a) redness, bulging, perforation, retraction, or decreased mobility of TM
b) bullae on TM (mycoplasma infection)
c) pain on palpation of the auricle or tragus
3. Administer appropriate hearing tests: Weber’s test, Rinne test (Figure
1-2), and 2-to 3-foot whisper 4. If the patient is hard of hearing, ask the
patient to hum
a) conductive defect: hum is louder in the affected ear
b) sensorineural defect: hum is louder in the unaffected ear
E. Nose: examine the nasal septum and nares for mucosal color, polyps,
perforations, and presence of swelling
F. Oropharynx: inspect the lips, gums, teeth, tongue, buccal mucosa,
uvula, and pharynx
1. Determine the “grade” of tonsils
1+: barely extend beyond the tonsillar pillars
2+: extend halfway to the uvula
3+: touch the uvula
4+: tonsils touch each other

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 a) peritonsillar abscess
b) exudative pharyngitis
c) palatine petechiae
d) postnasal drainage
2. Determine the presence of partial plates, full dentures, caries, if any
G. Palpation
1. Over sinuses (e.g., over maxillofrontal areas, mastoids, C2) for pain or
pressure 2. Neck
a) lymphadenopathy with or without tenderness (Figure 1-3) b) thyroid
abnormalities
V. Respiratory

A. Observe the chest for AP and lateral diameter and deformities B.

Auscultate the anterior and posterior chest and right lateral chest
(Figure 1-4)
1. Rales: fine, crackle sounds that can be associated with fluid in the
airways or with fibrosis 2. Rhonchi: coarser sounds, as with someone
who needs to cough; often clears with cough 3. Stridor: high-pitched
inspiratory sound associated with laryngeal spasm 4. Wheeze: low-
pitched inspiratory or expiratory sound associated with bronchospasm
or pulmonary congestion
C. Examine the chest, including respiratory excursion, and perform
bronchophony, egophony, and whispered pectoriloquy, if indicated D.
Percuss posterior lung fields
1. Dullness indicates consolidation (e.g., pneumonia, pleural effusion) 2.
Hyperresonance (consider emphysema or pneumothorax)
E. Percuss diaphragmatic excursion and palpate for vocal fremitus, if
indicated F. Examine capillary refill in the nailbeds
1. Capillary refill >3 seconds
VI. Chest/Cardiovascular

A. Palpate the precordium

1. Thrills, heaves (left ventricular [LV] dysfunction: apical; right
ventricular [RV] or left atrial [LA] dysfunction: parasternal), or lifts 2.

19
 Displacement of PMI
B. Inspect breasts for skin redness, dimpling, or puckering; specifically,
inspect while the woman (1) places her hands on her hips and shrugs
her shoulders and (2) presses her palms together over her head C.
Palpate breasts and axillary, supraclavicular, and epitrochlear nodes
(with the patient in the supine position)
1. Abnormal skin changes
2. Nodules or lymphadenopathy
3. Nipple discharge
4. Supraclavicular nodes
D. Auscultation (Figure 1-5)
1. Listen over the precordium with the patient seated upright and
leaning forward, in the supine position, and in the left lateral position
2. Use both the bell and the diaphragm
3. Listen for S1 and S2 (including splits); to identify S1, time it with the
carotid pulse
a) split S1 is usually normal; best heard in the tricuspid area b) split S2 is
physiologic (normal) if it resolves with deep expiration (i.e., it is
“blown away”) c) paradoxical split S2: consider left bundle branch
block (LBBB) or aortic stenosis d) fixed split S2: consider atrial septal
defect e) murmurs (also see murmurs in Chapter 8 and Table 8-1) f)
clicks
g) loud S2 means increased peripheral resistance, regardless of BP
measurement; requires aggressive treatment h) opening snap
i) friction rubs
j) S3 or S4 (see Figure 8-1)
4. Listen over the carotid arteries, abdominal aorta, and renal and
femoral arteries
a) bruits: record presence or absence (presence may indicate renal artery
stenosis or abdominal aortic aneurysm)
E. Inspect the neck (with the head of the bed at a 45-degree angle) for
carotid and internal jugular venous pulsations and jugular venous

20
 distention (JVD)
1. JVD elevated >2 cm above the clavicle (would mean a pressure of >7
cm because the clavicle is approximately 5 cm above the right atrium)
2. Visible jugular veins that do not collapse with inspiration
(Kussmaul’s sign)
F. Palpation
1. Check the carotid pulses (individually)
2. Check the abdomen for hepatojugular reflux and aortic pulsation
a) widened aortic pulsation
3. Check the peripheral pulses for rate, rhythm, and amplitude (Figure 1-
6)
a) absence of pulse(s)
b) exaggerated, widened femoral pulse (consider femoral aneurysm)
4. Check the lower extremities for edema
a) nonpitting edema: consider lymphatic obstruction or hypothyroidism
b) pitting edema: consider right sided HF, cirrhosis, renal disease, or
venous insufficiency (edema may be asymmetrical with venous
insufficiency)
VII. Abdomen

A. Inspection
1. For contours and scars
2. Purple striae indicative of Cushing’s syndrome (see Chapter 16) 3.
Have the patient raise his or her head and shoulders off the table
a) hernia
b) masses
4. For engorged veins (consider hepatic cirrhosis or inferior vena cava
obstruction) 5. For distention (consider ascites or abdominal tumor)
B. Auscultate for bowel sounds
1. High pitched, tinkling (consider intestinal obstruction) 2. Decreased or
absent (consider paralytic ileus or peritonitis)
C. Percussion

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 1. Liver and splenic borders
a) hepatosplenomegaly
2. Other areas as necessary
3. Costovertebral angle tenderness (CVAT): the patient must sit for this
test
a) positive test (pain on examination)
D. Palpation
1. Light
a) peritoneal irritation
2. Deep
a) liver or spleen palpable or tender
b) masses
c) aortic pulsation >2.5 cm (consider aortic aneurysm)
3. Rebound tenderness
a) acute abdomen (see Chapter 10)
4. Inguinal nodes
a) infection
b) malignancy
E. Rectal examination (if indicated)
1. Rectal masses
2. Fecal retention
3. Abnormal prostate
4. Positive guaiac
VIII. Genitalia: male

A. Check for inguinal hernia

B. Check the skin (including the ventral side of the penis) for any lesions
C. Testicular examination (teach self-testicular examination)
1. Undescended testicle
2. Right testis lower than the left (consider situs inversus or renal cell

22
 cancer; obtain renal U/S) 3. Epispadias, hydrocele, varicocele (refer to a
urologist)
IX. Genitalia: female

A. Urethra: check for discharge and erythema

B. External genitalia
1. Inspect hair pattern
2. Observe for lesions
3. Determine the presence and condition of the hymen
4. Perineal support: spread the labia and have the patient “bear down”;
inspect for drainage and rectocele or cystocele
a) lesions
b) abnormal discharge
C. Palpate Bartholin’s, urethral, and Skene’s glands for pain, swelling,
drainage D. Perform vaginal examination
1. Inspect by inserting a speculum to visualize the cervix and vaginal
walls (lubricate with warm water, if needed; may use K-Y if not
obtaining a Pap) 2. Inspect vaginal walls for color, discharge, rugae,
and lesions 3. Inspect the cervix for color, parity, lesions, discharge,
friability; note the cervical os size and position and lesions 4. Obtain
indicated cultures and Pap smear (if done separately, GC/CT cultures
should be obtained before the Pap smear); perform a wet prep, if
indicated (see the following section, “How to Do a Wet Prep”)
E. Bimanual examination (palpation)
1. Cervix for contour, smoothness, cervical motion tenderness 2. Uterus
for size, shape, position, and consistency (Figure 1-7) 3. Adnexa for
size, presence of masses, and tenderness; if unable to palpate,
document such; it is often difficult to palpate adnexa in larger women
4. Cervical motion tenderness (consider pelvic infection or
inflammation) 5. Enlarged or tender uterus
6. Adnexal fullness or tenderness
F. How to do a wet prep
1. Items needed: Pap smear spatula; two cotton-tipped applicators; two
capped test tubes, one with 1 to 2 ml of saline and one with 1 to 2 ml of

23
 KOH solution; nitrazine paper; two slides with slide covers 2. Obtain
specimens from the lateral wall of the vagina; place one of the
applicators in each of the test tubes 3. Use the specimen on the spatula
to check vaginal pH with nitrazine paper (normal is <5) 4. Perform a
“whiff” test by smelling the applicator in the KOH tube; the result is
considered positive if there is an “amine” or fishy odor 5. If pH is
normal and whiff is negative, no further testing may be needed for
bacterial vaginitis (BV) 6. Microscopic evaluation
a) to check for BV, trichomoniasis, or Candida infection (yeast) using the
applicator, place a few drops from the saline tube on one slide and top
with a slide cover; repeat with the KOH tube applicator on the other
slide b) view under high power to look for epithelial cells, WBCs, clue
cells, lactobacilli, or trich on saline-prepared slide; look for yeast buds
and hyphae on KOH-prepared slide (Figure 1-8)
X. Musculoskeletal

A. Observe gait
1. Abnormal gait
B. Inspect joints for redness, increased heat, painful range of motion
(ROM) C. Examine the back for abnormal curvatures and document if
present
1. Scoliosis
2. Kyphosis
XI. Neurological system (may be integrated with the rest of the examination)

A. Cognitive status
1. Evaluate for orientation to person, place, and time
2. Determine judgment and problem-solving abilities: ask, “If you smell
smoke in the house, what do you do?”
3. Test abstract thinking: ask the patient to explain a proverb such as “A
stitch in time saves nine.”
4. Evaluate affect: behaviors that may signify depression or mood lability
(see Table 3-10 for an example)
B. Language
1. Test verbal abilities, namely, speech patterns, fluency, and content

24
 a) speech disturbances (Table 1-1)
2. Test the ability to write and copy
3. Check gestures and the ability to follow serial and three-step
commands; for example, ask the patient: “Hold up your right hand,
stick out your tongue, and close your eyes.”
4. Check whether the patient has appropriate recognition skills (i.e., the
ability to name common objects) 5. Check reading ability and
comprehension
a) agraphia (inability to write)
b) alexia (inability to read, if the patient was previously able to read)
C. Vision
1. See HEENT section, C.1 for a description of visual acuity examination
2. Ophthalmologic examination (Tables 1-2 and 1-3)
D. Sensory: head and neck
1. Always test right and left separately
2. Check tactile ability: ask the patient to identify the body part being
touched 3. Test auditory ability: Rinne and Weber’s tests (see Figure 1-
2) and sound comprehension
E. Motor
1. Gait
2. Test muscle strength
a) upper extremities: shoulder abduction, elbow and wrist flexion and
extension b) lower extremities: hip and knee flexion and extension,
ankle dorsiflexion and plantar flexion
3. Grading scale for motor (muscle) strength:
5 = normal
4 = weak but able to resist the examiner
3 = moves against gravity but cannot resist the examiner
2 = moves but unable to resist gravity
1 = flicker but no movement

25
0 = no movement
4. Staggering, unsteady, wide-based gait (ataxia): test with tandem gait;
should be able to walk in a straight line 5. Inability to execute
volitional activity (apraxia)
F. Cranial nerve (CN) examination (Table 1-4)
1. CNS lesions cause contralateral facial weakness below the eyes (the
forehead is spared) 2. Peripheral CN VII lesions may cause complete
facial weakness (including the forehead)
G. Coordination
1. Ability to perform rapid alternating movements—have the patient
alternately pronate and supinate the hand against a stable surface (e.g.,
a table or patient’s own thigh); inability to complete this test
(dysdiadochokinesia) 2. Finger-to-nose: ask the patient to touch his or
her nose and the examiner’s finger alternately with rapid repetition;
observe for accuracy and tremor 3. Heel-to-shin: have the patient place
his or her heel on the opposite knee and slide the heel down the shin to
the foot; observe for accuracy and tremor 4. Romberg’s test: have the
patient stand with his or her feet together and eyes open for 20 to 30
seconds and then with eyes closed for 20 to 30 seconds (there should
be minimal, if any swaying). Then check pronator drift: while
continuing to stand with eyes closed, have the patient raise his or her
arms straight forward with the palms up and hold for 30 seconds (both
arms should remain in position); then gently press down on each wrist
and the arm should return to the previous position.
5. Inability to perform any of the tests
6. Tremors
H. Gait
1. Ask the patient to walk forward on heels and backward on tiptoes 2.
Observe tandem gait (ability to walk a straight line, as if on a
tightrope) 3. Foot drop
4. Spasticity or bradykinesia
I. Sensory: peripheral
1. Compare right and left sides with the patient’s eyes covered or closed
2. Definitions

26
 a) hyperesthesia: excessively sensitive to touch
b) paresthesia: sensations without stimulation from the examiner
3. Evaluate the patient’s ability to discern the following:
a) vibration: use a tuning fork on the DIP joints of both thumbs and both
big toes b) light touch: use a wisp of cotton
c) stereognosis: patient recognizes an item placed in the hand (e.g., a
quarter) d) two-point discrimination: touch the patient in various
places at the same time using sharp and dull objects and note any
differences; if felt on only one side, CNS sensory deficit is present on
the opposite side of the brain e) temperature: blow gently on the
patient’s skin (medial wrist is best) with lips apart (warm) and lips
pursed (cool); may also use very warm and cold water in test tubes
4. Inability to discern any of these sensory tests
J. Reflexes
1. Assess for symmetry

Reflex Level Normal Response

Biceps, A C5-C6 Elbow flexion
Triceps, B C7 Elbow extension
Brachioradialis, C C6-C7 Wrist flexion
Patellar, D L3-L4 Knee extension
Achilles, E S1 Foot extension

Scoring: 0, absent; 1+, weak; 2+, normal; 3+, exaggerated; 4+, clonus

2. Check for DTRs: the joint being tested should be at approximately 90

degrees and fully relaxed 3. In patients with altered LOC or possible
CVA or paralysis, the following reflexes may also be checked:
a) abdominal: stimulate above and below the umbilicus; normally, the
umbilicus moves toward the side stimulated
b) plantar: stimulate the sole of the foot from the heel to the big toe with
a blunt object; normally, the toes flex; a positive (abnormal) Babinski’s
sign occurs when the big toe moves up and the toes fan out
4. Comparison of central and peripheral nervous system lesions (Table 1-

27
5)

FIGURE 1-1 ​Right Tympanic Membrane. Source: (From Black, J., & Hawks, J.H.
[2009]. Medical-Surgical Nursing, 8th ed. Philadelphia, Elsevier.)

28
FIGURE 1-2 ​Rinne and Weber’s Tests.

29
FIGURE 1-3 ​Lymph Nodes of the Head and Neck. Source: (From Seidel, H., et
al. [2011]. Mosby’s Guide to Physical Examination, 7th ed. Philadelphia, Elsevier.)

FIGURE 1-4 ​Lung Lobes and Breath Sounds. Source: (From Bontrager, K.
[2009]. Textbook of Radiographic Positioning and Related Anatomy, 7th ed. Philadelphia,
Elsevier.)

30
 FIGURE 1-5 ​Heart Auscultation Sites.

FIGURE 1-6 ​Peripheral Pulses. Source: (From Harkreader, H., Hogan, M., &

31
 Thobaben, M. [2007]. Fundamentals of Nursing, 3rd ed. Philadelphia, PA: Elsevier.)

FIGURE 1-7 Cervix and Uterus Positions. A, Anteverted; B, anteflexed;

C, retroverted; D, retroflexed; E, midposition. Source: (From Seidel, H., et al.
[2011]. Mosby’s Guide to Physical Examination, 7th ed. Philadelphia, Elsevier.)

32
 FIGURE 1-8 ​Microscopic Findings for Wet Prep.
Table 1-1
Speech Disturbances: Characteristics and Pattern

Speech Disturbance Characteristics

Fluent aphasia (Wernicke’s area) Lacks content
Unable to comprehend spoken words and
phrases
Unable to repeat or name objects
Nonfluent aphasia (Broca’s area) Slow, scanning speech
Intact comprehension
Impaired writing ability
Inability to verbally express thoughts
Global aphasia (both Broca’s and Wernicke’s Nonfluent speech
areas) Unable to comprehend, read, or write
Unable to name objects

Table 1-2
Ophthalmologic Examination

Finding Characteristics Possible Causes

Normal Yellow-white disc
Well-defined disc margins
Arteries (smaller) enter and veins (larger) leave at the optic disc

Papilledema Edema of the optic disc: unilateral if inflammatory (may have a Lesions that
sudden loss of vision in the inflammatory state); usually increase
bilateral if noninflammatory Impaired visual acuity in the intracranial
chronic stage pressure

33
 Encephalopathy
Optic artery
aneurysm or
cavernous
sinus
thrombosis
Guillain-Barre
syndrome

Optic Decreased vision Optic neuritis

atrophy Optic disc white or gray-white Neurosyphilis
The cup may be absent Trauma to the
orbit
Toxins or
poisons
DM

Table 1-3
Eye Signs

Eye Sign Characteristics Pathology

Normal Pupils 3-4 mm, symmetrical, round,
findings and reactive to light and
accommodation Palpebral fissure 8-12
mm and symmetrical

Adie’s pupil Unilateral, large pupil Post viral infection

Sluggish constriction to prolonged light Loss of parasympathetic reactions
exposure
Direct light reflex absent

Anisocoria Unequal pupil size May be a normal variant if the

Reactive to light and accommodation difference is <1 mm
Compression of CN III (e.g.,
aneurysm, cerebral herniation)

Argyll Pupils smaller than normal in dim light Neurosyphilis, viral encephalitis
Robertson Minimal dilation, often unequal Lesion in midbrain
pupil
Pupils may appear irregular DM
Visual disturbance

Dysconjugate Inability to follow a moving finger in Space-occupying lesion

gaze all eye fields Neuromuscular disorders
Deviation of eye
Frontal lobe dysfunction (dementia or

34
 Lack of gaze coordination trauma)
DM

Marcus Gunn Pupils equal, with positive direct light Optic nerve involved (e.g., with
pupil reflex multiple sclerosis)
Pupil dilates when direct light is
moved from the intact eye to the eye
with the abnormal pupil

Nystagmus Involuntary, oscillating eye movements May be associated with strain

May occur at rest or during eye field
examination
May be vertical or lateral
secondary to poor lighting
Side effect of certain drugs (e.g.,
phenytoin, alcohol, barbiturates)
Bilateral nystagmus may indicate
myasthenia gravis

Ptosis Palpebral fissure <5 mm CN III palsy

Asymmetrical Myopathy
Neuromuscular disorders (e.g.,
myasthenia gravis)
Atonic eyelid muscles
Inflammatory lesion of the eyelid

Table 1-4
Cranial Nerve Examination

Cranial Nerve Type and Function Tests Abnormal Findings

Olfactory Sensory: Do not use ammonia Obstructive nasal
Smell Test each nostril separately passage
with alcohol preparation, Lesions of the frontal
mint, and coffee lobe, pituitary uncus,
or hippocampal gyrus
Optic Sensory: Snellen’s chart Amaurosis (loss of
Central and peripheral Newspaper print vision); refer
vision Color vision immediately
Count fingers in peripheral Cataracts
fields Cortical blindness
Ophthalmoscopic Papilledema
examination Optic atrophy
Oculomotor Motor: Pupil size, symmetry, Ptosis
Pupillary constriction shape, and accommodation Nonreactive pupil
Eyelid elevation Anisocoria
Optic nerve lesions
Trochlear Motor: Follow a finger or object in Nystagmus*
Eye movements all planes (EOMs) Diplopia
Dysconjugate gaze

35
Trigeminal Sensory & motor: Pinprick to face with eyes Loss of sensation,
Tongue and facial closed paresthesia, or pain
sensation Have the patient open and Deviation of jaw
Corneal reflex close the jaw Lack of blink reflex
Corneal reflex (use a drop
of saline)
Abducens Motor: (Test with CN III and IV)
Lateral eye movement
Facial Sensory & motor: Have the patient wrinkle
Asymmetry of face
Facial expression the forehead, grimace, raise
Salivary and lacrimal eyebrows, smile, and frown Deviation of mouth
glands Taste: sweet, sour, and Weakness of forehead
Taste bitter substances to the
Inability to close eyes
anterior tongue
Loss of taste
Excessive tearing
Acoustic† Sensory: Rinne and Weber’s tests Unilateral deafness
Hearing Whisper Tinnitus
Equilibrium Ticking watch Lateralization
Equilibrium Vertigo, dizziness, or
ataxia
Glossopharyngeal Sensory & motor: Taste: sweet, sour, and Loss of taste
Taste on the posterior bitter substances to the Loss of gag or
tongue posterior tongue Gag and swallow
swallow
Gag or swallow Dysphagia
Vagus Sensory & motor: Gag Inspect the soft palate Loss of voice or
or swallow hoarseness
Uvula in the midline
Stimulate the pharyngeal Deviation of uvula
wall Coughing and
Voice quality choking

Accessory Motor: Palpate trapezius and Paralysis or weakness

Fluid movement of the
sternocleidomastoid Atrophy
head and neck in muscles
flexion, extension, and Spasticity
rotation Have the patient turn the
head against resistance
Have the patient shrug the
shoulders against
resistance
Hypoglossal Motor: Tongue Have the patient move the Spastic paralysis
movement tongue side to side Deviation from the
Observe for symmetry and midline
rhythmicity Dysarthria

36
 Spastic speech

*Marked
nystagmus on lateral gaze or any nystagmus on vertical gaze suggests a peripheral or CNS lesion.
†Ask the patient to hum if he or she has decreased hearing: if the hum is louder in the affected ear, this would be a conductive defect; if
the hum is louder in the unaffected ear, this indicates a sensorineural defect.

Table 1-5
Distinguishing Central and Peripheral Lesions

Upper Motor Neuron (CNS) Lower Motor Neuron (Peripheral)

Deep tendon reflexes (DTRs) Increased Decreased
Muscle tone Increased Decreased
Atrophy Not usually Yes
Fasciculations No Yes
Babinski’s reflex Present Absent

37
Focused examinations
Respiratory

I. Emphasis on history of present illness

A. SOB, dyspnea, orthopnea, and nocturnal dyspnea

B. Wheezing
C. Cough, sputum, and hemoptysis
D. Sore throat
E. Earache
II. Past medical history

A. Asthma (include ED visits and hospitalizations)

B. Bronchitis or COPD
C. Pneumonia or TB
D. Frequent strep throat or ear infections
E. Chest trauma or spontaneous pneumothorax
F. Occupational exposure and tobacco use
G. Last influenza or pneumonia vaccine, TB test
H. Current or past history of smoking (of any type)
III. Family history

A. Asthma
B. Chronic airway disease
IV. Examination findings that should not be missed

A. Fingernail clubbing
B. Cyanosis
C. Prolonged expiration
D. Tachypnea at rest
E. Abnormal, absent, or decreased breath sounds
F. Pleural friction rub

38
 G. SOB or use of accessory muscles to breathe
H. Unequal inspiration/expiration contours of the right and left sides of
the thorax
V. Referral guidelines (urgent)

A. To ED: patients in acute distress or with suspected epiglottitis (see

Chapter 17) B. To ED or ENT: peritonsillar abscess
VI. Include cardiovascular and abdominal examinations in case of respiratory complaints

Cardiovascular

I. Emphasis on history of present illness

A. Cardiac (e.g., chest pain, palpitations, dysrhythmias, tachycardia,

cyanosis, cough, exertional dyspnea, orthopnea, nocturnal dyspnea,
edema, dizziness, syncope, diaphoresis) B. Vascular (e.g., phlebitis,
intermittent claudication, skin color changes, cold or painful
extremities)
II. Past medical history

A. Rheumatic fever
B. Murmurs
C. Mitral valve prolapse (MVP)
D. Ischemic heart disease (e.g., angina, MI, stent placement, PTCA, heart
surgery) E. Dysrhythmia (e.g., atrial fibrillation)
F. HF
G. CVA
H. HTN
I. Hyperlipidemia
J. DM
K. Gallbladder disease
L. Peptic ulcer
M. DVT
N. Marfan syndrome
III. Family history

39
 A. Sudden death of a family member before age 55
B. CAD
C. HTN
D. Raynaud’s disease or other peripheral vascular diseases E. DM
IV. Examination findings that should not be missed

A. Dyspnea on exertion
B. Change in the usual heart rhythm or rate
C. New or worsening murmur
D. S3 and/or S4
E. Jugular venous distention (JVD)
F. Hepatomegaly
G. New bruits
H. Widened aortic pulsation >2.5 cm (consider abdominal aortic
aneurysm) I. Chest pain indicating possible MI, PE, or aneurysm (see
Table 8-4)
V. Referral guidelines

A. Chest pain of cardiac origin (e.g., suspected MI or new angina) B.

Suspected aortic dissection
C. Pulmonary embolism
D. New or refractory HF
E. Acute arterial insufficiency
F. Suspected DVT
G. Symptomatic childhood or adult murmurs
VI. Include respiratory and abdominal examinations in case of cardiovascular complaints

Abdominal

I. Emphasis on history of present illness

A. Onset and changes (e.g., worsening, more constant)

B. Characteristics (e.g., sharp, crampy, dull)
C. Associated symptoms (e.g., nausea, vomiting, diarrhea)

40
 D. Presence or absence of appetite and fever
E. See Figure 10-1, for pain sites F. Review of 24-hour dietary intake and
presence of similar symptoms in the patient’s family
II. Past medical history

A. Usual elimination patterns

B. Ulcer
C. Irritable bowel syndrome or inflammatory bowel disease
D. Gallbladder disease
E. Abdominal operations (open and laparoscopic)
F. Women: LMP, type of contraception used
G. Recent travel
III. Family history of GI tract disorders
IV. Examination findings that should not be missed

A. “Acute abdomen”
B. Hepatomegaly
C. New bruits
D. Pulsating mass
E. Pregnancy
V. Referral guidelines

A. Patients with an initial diagnosis of hepatic cirrhosis or Cushing’s

disease B. Symptoms suggestive of an acute abdomen or aortic
aneurysm C. Any abdominal bruit (may obtain appropriate ultrasound
first) D. Rectal mass or inguinal lymphadenopathy
VI. Include respiratory and cardiovascular examinations in case of abdominal complaints; also
include pelvic examination, if indicated (e.g., lower abdominal pain in a woman of childbearing
age)

Routine well-woman examination

I. Emphasis on history of present illness

A. Menstrual history (age at menarche, LMP, age at menopause) B.

Sexual history (age at first intercourse, number of sexual partners,
STIs) C. Obstetric history (number of pregnancies, live births,

41
 abortions/miscarriages) D. Use of contraception (ask: “what do you do
to prevent pregnancy?”)
II. Past medical history

A. Gallbladder disease
B. Heart disease
C. Varicose veins
D. History of abnormal Pap smears, date of last Pap smear
E. Menopausal symptoms, dyspareunia, vaginal discharge, lesions,
incontinence F. Last mammography (and BMD, if indicated)
G. Nutritional history
III. Family history

A. Breast or reproductive tract cancer

B. Heart disease
C. HTN
D. DM
E. Osteoporosis
F. Thyroid problems
IV. Referral guidelines

A. To ED: abdominal pain; may/may not have spotting (suspected

ectopic pregnancy) B. To OB/GYN: suspected malignancy (e.g.,
uterine, ovarian, vulvar)

Sports physical examination

I. Goals of the examination include the following:

A. To identify problems carrying risks of life-threatening complications

during participation (e.g., hypertrophic cardiomyopathy) B. To
maximize safe participation in sports
C. To identify conditions requiring a treatment plan (e.g., HTN) D. To
identify and treat old musculoskeletal injuries
E. To identify and treat conditions that can interfere with performance
(e.g., exercise-induced bronchospasm) F. To remove unnecessary

42
 restrictions on participation
II. The emphasis of history and examination is on cardiovascular, respiratory, and
musculoskeletal systems. The medical history is the most sensitive and specific part of the
examination for detecting possible condition(s) that would restrict or exclude participation.

A. Each school or organization will have an evaluation form to be

completed for sports participation
1. The history section is completed by the athlete or parent/guardian; the
provider reviews this with the athlete and writes comments on any
positive answers 2. The history section includes questions about
symptoms/signs suggesting possible serious medical conditions 3. The
physical examination section is completed by the provider (or
providers if the examination is completed by more than one person)
B. For the history of past injuries, ask about the following:
1. Previous exclusion from sports for any reason
2. Length of time lost from participation
3. Current sequelae of the injury
4. Any loss of consciousness or amnesia after a head injury
C. Most children and teens with chronic medical conditions can
participate in sports at some level after evaluation and treatment. (See
Referral guidelines and Conditions requiring a treatment plan later in
this section.) D. Sudden cardiac death (SCD) is disproportionately
more common in males. Cardiovascular conditions that predispose
individuals to SCD are rare and difficult to treat.
III. Physical examination is directed by the form used; components are included for evaluation
because if present, further evaluation is required

A. Musculoskeletal
1. Full neck ROM (pain with or restriction of movement requires further
evaluation) 2. Asymmetrical shoulder height
3. Swelling of any extremity
4. Limited shoulder ROM
5. Asymmetry or loss of motion with elbow ROM (especially if the
student is involved in throwing sports) 6. Inability to “duck walk”
7. Inability to hop 5 times on each foot without ankle pain or instability

43
 B. Cardiovascular
1. Vital signs (“normal” ranges depends on the age of the athlete; some
states also have guidelines) 2. Ideal body weight (<85th percentile)
3. ECG if a FH of atrial fibrillation, SCD, or arrhythmia is present or if the
athlete has a history of tachycardia that does not resolve with rest
C. Concussions
1. There are no evidence-based guidelines regarding return to play for
athletes aged 5 to 18 years 2. Worrisome signs include the following:
a) prolonged recovery time
b) shorter intervals between concussions
c) progressively less force to cause a concussion
d) providers may check for current guidelines at
www.cdc.gov/concussion/clinician.xhtml
IV. Referral guidelines: athletes with the following symptoms or conditions should be evaluated
by a specialist before participation in sports activities

A. Cardiac
1. HTN (see Table 2-3) 2. Undiagnosed systolic heart murmur louder
than grade 2/6
3. Any bruits
4. Complaints of dyspnea on exertion, fatigue, atypical or angina chest
pain, presyncope or syncope (especially during or immediately
following exertion), palpitations, lightheadedness; these can be
symptoms of hypertrophic cardiomyopathy (formerly called idiopathic
hypertrophic subaortic stenosis [IHSS]), coronary artery anomalies,
dysrhythmias, or Wolff-Parkinson-White syndrome 5. Personal or
family history of Marfan syndrome
6. Family history of sudden death before 55 years of age (including
drowning)
B. Musculoskeletal
1. Restriction/limitation of joint ROM or painful ROM of joint; inability to
“duck walk”
2. Down’s syndrome with atlantoaxial instability

44
 3. Cerebral palsy or muscular dystrophy
C. Neurological
1. History of head or spinal trauma, craniotomy, severe or repeated
concussions 2. Poorly controlled seizure disorder
D. Miscellaneous
1. Loss of an eye or the best vision in the good eye is worse than 20/40
2. History of detached retina, previous eye surgery, or serious eye injury
3. Absent kidney or testicle
4. Enlarged liver or spleen associated with a systemic disease 5.
Malignancy
6. Organ transplant recipient
7. Sickle cell disease
8. Bleeding disorders
9. Uncontrolled DM
10. Pregnancy
11. Eating disorders (e.g., anorexia nervosa or bulimia)
V. Conditions requiring a treatment plan before or during exercise

A. Exercise-induced bronchoconstriction
B. HTN
VI. There is no conclusive evidence that the following supplements will enhance athletic
performance, and they may cause physical problems*

A. Creatine
1. Increases muscle size by causing water retention, not by adding
muscle 2. Does not seem to increase endurance or improve
performance
B. Amino acids: no evidence that they improve performance or increase
lean body weight more than regular food C. Caffeine
1. May increase endurance and time to exhaustion
2. Doses of 250 mg/day can cause insomnia, tachycardia, nervousness, GI
complaints (each energy “shot” contains 100 to 350 mg caffeine) 3.
NOTE: 800 mg caffeine will cause failure on the NCAA drug test

45
 D. Dimethylamylamine
1. No evidence that this works
2. Can cause cardiac toxicity when used with other stimulants (e.g.,
ADHD medications, pseudoephedrine, caffeine) 3. Can cause a false-
positive drug test (related to amphetamine)
E. Bitter orange: not safe (linked to CVA, MI, dysrhythmias, and death)
F. DHEA (dehydroepiandrosterone)
1. Not proven to improve muscle mass or strength
2. Can increase estrogen and testosterone levels

*The
suggested format assumes that the patient is in a stable condition. The order should be modified as the patient’s condition
warrants. In cases of acute illness, the initial focus is on the affected and related body systems, with emphasis on the history of the
present illness.
*From
Prescribers’ Letter, Natural Medicines used for Improving Athletic Performance.

46
CHAPTER 2

47
Pediatric assessment
I. The goals of pediatric assessment are as follows:

A. To record and monitor overall growth and development from birth

through late adolescence B. To identify problems with the patient’s
psychosocial maturity and problem-solving abilities C. To identify any
genetic anomalies and seek appropriate referral when necessary D. To
verify attainment of age-related milestones
E. To note any deviations or problems that the parent/caregiver has
identified
II. Your assessment should always consist of normal patterns of development, and when illness
is considered, you should identify deviations from normal patterns as the cause of illness III.
Your approach to pediatric assessment depends on the goal of the encounter: is this a well-child
checkup or illness visit, and how severe is the illness at this time? Does the child need urgent
referral to ED?

A. Identifying the problem is the most difficult issue; the infant/toddler

cannot tell you specifically what the problem is in words, and many
times the caregiver also cannot identify the presenting problem;
however, as the child matures, the problems are easier to identify B.
Always try to establish a rapport with both the caregiver and the child;
pediatric assessment relies heavily on the trust between the caregiver,
pediatric patient, and practitioner
IV. Assessment findings vary with each visit, depending on the stage of growth and
development exhibited by the infant/child/adolescent V. Inspection is the most important clue;
your eyes and ears are the best tools for assessment

P r a c t i c e Pe a r l s f o r H e a l t h H i s t o r y

• Observe the caregiver and patient’s relationship.

• Always assume a very calm and matter-of-fact attitude; children know when you are
uncomfortable or nervous.
• A quiet room with some minor distractions for the child (e.g., coloring books, reading books,
handheld toys/games) is helpful while the practitioner is questioning the caregiver.

48
 • Always allow the toddler/child some personal space during the interview; this will facilitate
trust with the examiner.
• Allow the infant/toddler/child to sit with the caregiver during the interview and as much as
possible during the initial examination.
• Use puppets or stuffed animals to distract toddlers/children while examining them and
allow them to hold objects during the examination if needed.
• Suggested examination techniques

• Infant on the examination table

• Preschooler on the parent’s lap
• Older child on the examination table
• Adolescent alone in the room, if possible
• Try to compliment the toddler/child/adolescent on something, whether it is clothes, hair, or
a toy. Ask older children questions about why they think they are here to be examined and
allow them to answer as much as they can.
• Initially, when you first touch the child, always touch nonthreatening body parts first, such
as head/hair, legs, or feet.
• If child is cooperative, examine pertinent body areas (e.g., heart, lungs, and ears) first
because children do not remain quiet for very long.
• Examine painful or stressful areas last (e.g., ears, genitals, or areas of pain).
• During the encounter, as the infant/child is being undressed, watch for ROM, symmetrical
movement, strength of extremities, balance, and symmetry of gait.

Comprehensive health history

I. Document the patient’s name, age, birth date, sex, and ethnic background at the time of the
visit II. Identify current living arrangements/situation (e.g., lives with parent[s] or foster care) III.
Chief complaint or reason for the visit

A. Try to elicit the child’s (4-year-old children can usually give some
valid information) and caregiver’s perspectives of the problem or
reason for the visit B. The caregiver may have other reasons for
seeking health care besides the scheduled visit
IV. History of present illness

A. A well-child visit focuses on growth and development, assessing

developmental milestones, nutritional habits, and safety in the home
and during outside activities, as well as the immunization status and
current medications, including OTC and herbal products B. An
episodic illness examination focuses on the specific reason for the visit.
The following questions are related to an episodic illness:

49
 1. Onset of symptoms: sudden, gradual, or episodic, and when
symptoms began
2. Type of symptom: pain, itching, fever, and change in appetite, feeding
pattern, or sleep pattern 3. Location of symptom: generalized or
localized
4. Duration/severity: how long have the symptoms persisted, are they
continuous or episodic, how have they affected daily routine or school
attendance?
5. Influencing factors: what makes the pain/symptom better or worse and
is there a precipitating factor or any new exposures to illnesses or
allergens 6. Past evaluation of this problem (e.g., lab values, x-rays,
past examinations and findings) 7. Past or current treatment(s)
a) what has been prescribed and what OTC medications have been used
or are currently being used to control symptoms?
b) are these medications working?
c) are other therapies being tried and what responses have occurred?
8. The physical examination and treatment will depend on the specific
system in question
V. Review of the past medical history is important at all visits

A. Prenatal history (of the mother)

1. Health during pregnancy (e.g., HTN, edema, gestational DM)
2. Any history of drug, alcohol, or tobacco use
3. Obstetric history of this and previous pregnancies (e.g., gravida, para,
or abortions)
B. Birth and neonatal history, including any difficulty with delivery;
Apgar score (if known); preterm birth; intensive care stay and reason;
was the baby maintained on O2 for any length of time; were
hearing/vision screening performed at birth and what were the results;
when was the first hepatitis B immunization given?
C. Note growth, social and personal development
D. Were developmental milestones achieved on time (Table 2-1)?
E. At what age was the toddler/child toilet trained; if toilet trained, does

50
 the toddler/child have accidents and are they continent at night?
F. Any phobias
G. Grade and performance in school; any behavior problems at school
H. Type of discipline; problems identified at home, school, or in social
settings I. Attention span and perceived hyperactivity
VI. Nutritional status

A. Bottle-or breast-fed, number of feedings per day, and amount ingested

B. Does the infant seem satisfied after bottle-or breast-feeding?
C. Types of foods offered and how much the infant eats daily
D. When was the child started on whole milk and how much does the
child drink?
E. Current weight and any gain or loss over the last year
F. Food allergies and what symptoms are elicited
G. Any pica habits
VII. Sleep habits

A. Where does the infant/child sleep; in what position is the infant placed
for sleeping purposes?
B. Does the infant/child sleep all night?
1. Does the child sleepwalk and is there a safety plan for the child?
2. Does the child have nightmares/terrors?
3. Does the child snore, how loudly and how often (e.g., every night, few
times a week)?
C. Is there a safety plan in case of fire or other disasters?
VIII. Past illnesses/injuries

A. Any childhood illnesses/injuries; if so, what were they and how were
they treated?
B. Past hospitalizations/surgeries
C. Past blood or blood product transfusions
IX. Medication history

A. Use of any OTC, herbal, prescribed, or illicit medications; does the

51
 child like to take medications, and is this a risk at home; does the child
take vitamin/fluoride supplements B. Allergies to any medications or
environmental pollens/chemicals and what reactions occur; what
medications are used or have been used to treat allergies?
C. Immunization history and any problems with immunizations; obtain
written immunization record (see www.cdc.gov/vaccines for
recommendations for current immunization schedules)
X. Personal and social history

A. Name of the physician/pediatrician, dentist, or other health care

provider involved with the child’s care B. Home environment
(exposure to smoke, alcohol, drugs, or unsafe practices)
C. Leisure activities and physical activity; amount of time spent watching
television or playing computer or video games D. Habits such as nail
biting, temper tantrums, or hair pulling/twisting
XI. Family history and dynamics

A. Composition of the family

B. Congenital abnormalities or illnesses identified in the family; any
history of consanguinity (i.e., sexual relations with a first degree
relative) C. Interaction between the patient and caregiver, patient’s
interactions with siblings and playmates, patient’s interactions with
authority figures D. Parental satisfaction with the patient’s behavior
E. Is the child in a daycare, public or private school, or home-schooled?
XII. Review of systems

A. Try to obtain the caregiver’s and the patient’s perspectives on each

component of the review of systems; do they perceive any problems
and if so, what are they?
B. General constitutional symptoms: fever, chills, malaise, night sweats,
or weight changes C. Skin: eczema, dry patches, texture, pigmentation,
or fingernail growth
D. Head: abnormal hair growth/loss; H/A, dizziness, syncope or loss of
consciousness E. Eyes: color of eyes, changes in vision or squinting
during distance vision (possible need for glasses), crossed eyes, eye
injuries; any familial eye diseases F. Ears, nose, and throat: ear
infection, perception of hearing, response to loud noises, speech

52
 development, runny nose, mouth breathing and snoring, nosebleeds
G. Teeth: age of eruptions and number of teeth, cavities, extractions,
abscesses, and dental visits (Figure 2-1) H. Cardiopulmonary: chest
pain or SOB with activity, unusual posture during activity, cyanosis,
tachycardia; can the child keep up with peers during play?
I. Gastrointestinal: constipation, diarrhea, N/V, number and type of
stools/day, fecal continence, encopresis, appetite and weight changes
J. Genitourinary: enuresis, dysuria or hematuria, urinary continence; if
toilet trained, the age when continent during both day and night;
menstrual history, sexual activity, use of contraception/condoms;
circumcision status; sexual maturity (see Tanner’s staging, Box 2-1) K.
Musculoskeletal: weakness, balance and coordination, unusual gait,
swelling of joints or pain L. Neurological: headaches, dizziness, ataxia,
brain injuries, seizures, learning problems, attention span, caregivers’
perception of activity (e.g., hyperactivity), fainting M. Endocrine:
growth patterns and any asymmetrical growth in body, unusual
amounts of fluid intake, heat/cold intolerance, or purplish skin striae
N. Hematologic: anemia, easy bruising/bleeding
O. Lymphatic: any node enlargement, pain, or swelling
P. Psychiatric: depression, mood changes, hyperactivity/hypoactivity,
suicidal thoughts, or sleep disturbances

53
 FIGURE 2-1 ​Dental Chart.
Table 2-1
Developmental Milestones

Language/Cognitive Social and Emotional

Age Motor Development
Development Development
Birth- Kicks legs, flails arms, raises Cries initially and then begins to cry Becomes quiet with caregiver’s contact
1 mo head when prone when hungry, angry, or
uncomfortable

2 Holds head steady when Starts making sounds other than Reacts to bottle or breast
mos pulled into sitting position crying; smiles

3 Makes crawling movement; Continues with more different Keeps one hand on the bottle or breast

54
mos uses arms to start propping
self up; visually tracks
through the midline
4 Holds hands together, grasps Squeals, laughs, and coos; shows
mos toy interest in surroundings
5 Rolls over stomach to back;
mos reaches for objects
6 Rolls over back to stomach;
mos begins to transfer objects
from hand to hand
7-8 Sitting without support;
mos bears some weight on legs;
transfers objects and will let
go of objects at times when
asked
9-10 Pulls to stand; three-finger
mos pincer grasp; is able to stand “dada”; understands single words
longer toward end of 10 mos; such as “bye bye”
starts to creep on hands and
knees
11-12 Gets into sitting position
mos with little help; walks with
one hand held, starts
“cruising”; two-finger pincer
grasp and will release toy
when asked
15 Walks backwards; has
mos independent locomotion;
throws things; stacks two
items
18 Descends/ascends stairs with
mos help; throws ball over the
hand
2 yrs Runs well; goes up stairs
with alternating feet; uses
utensils to eat
3 yrs Stands on one foot for <1
min; starts trying to ride
tricycle; holds sippy cup with
one hand Rule of 3: 3 yr, 3 ft,
33 lbs; height 3-4 in/yr;
weight 4-5 lbs/yr
4 yrs Climbs well; hops on one
foot; cuts across paper
sounds, smiles spontaneously; is
more curious about surroundings
Orients to sounds
Babbles
Responds to name
Imitates sounds, begins “mama” and
Uses “mama,” “dada” specifically for
the caregiver; speaks one word (e.g.,
“no”); knows object permanence
Develops 18 sounds; knows objects
have purpose
Knows 10-50 words, 2-3 body parts;
enters into the “terrible twos,” throws tries to redress self
tantrums and becomes more stubborn
2-3-word sentences, understands
more concepts, begins to put puzzles
together; copies vertical and
horizontal lines; builds tower of three
blocks
300-500 word vocabulary; speech is
mostly understandable but may have
some phonological issues; magical
thinking; egocentric; knows age, sex,
and full name; asks questions; copies
circle
Vocabulary of 1500 words, uses 6-8-
word sentences and knows plurals;
knows one color; copies cross, draws
person with 2-4 body parts; uses
scissors
55
while feeding; begins to recognize and
smile at parents
Recognizes the caregiver by sight and
sound of voice and acts excited when the
caregiver is around
Smiles when the caregiver makes noises
Shows likes and dislikes; beginning of
“stranger anxiety”
“Stranger anxiety” continues
“Stranger anxiety”; begins to play “pat a
cake”; cries when objects are taken away
Comes when called; imitates actions;
cooperates with dressing
Helps undress self; feeds self finger foods
Partially feeds self; undresses self and
Refers to self as “I”; may start toilet
training; attaches to toys; feeds self
Uses toilet but needs help to wipe, stays
dry during the day and mostly at night;
washes hands by self; puts on shoes,
partially dresses self; starts to interact
with others of age and has imaginary
friends
Can tell a story; responds to two-part
commands, toilets independently but
may still have “accidents” at night;
brushes teeth with supervision, washes
hands independently; has cooperative
play with peers
5 yrs Swings; prints first name; Copies triangle and square, draws Responds to three-part commands;
skips, hops on alternate feet person with body parts; counts up to begins school separation
10 items and knows four colors

6 yrs Somersaults; ties shoes, Copies diamond; knows most of own Cooperative play, social and friendly
buttons shirt body parts

Box 2-1

Ta n n e r’ s S e x u a l M a t u r i t y R a t i n g
Pubic hair

1. Sparse, slightly darker hair along the labia and at the base of the penis 2. Hair darker,
coarser, curlier; spreading over the entire pubis
3. Hair thick and dark like adult; cover the pubis but not on thighs
4. Adult type and quantity; also on medial thighs

56
Breasts

1. Elevation of only the nipple

2. Breast bud; small mound of breast and nipple develop; areola widens
3. Breast and areola grow, but the nipple is flush with the breast surface
4. Areola and nipple form a second mound over the breast
5. Mature breast; only the nipple projects

57
Genitals

1. Same size and proportion as early childhood

2. Testes and scrotum begin to enlarge; scrotum reddens and changes texture

58
3. Testes and scrotum continue to grow; penis longer
4. Testes almost fully grown; scrotum darker; penis larger and broader (glans develops) 5.
Adult size and shape

59
Adapted from Engel, J.K. (2006). Mosby’s Pocket Guide to Pediatric Assessment, 5th ed. St. Louis: Elsevier; Blackwell, J.M. (1962). Growth
at adolescence. Oxford, England: Blackwell Publishing Ltd.

60
Guidelines for comprehensive pediatric
assessment
General observations
I. The overall physical examination for pediatrics is the same as that for adults, although there
are some variations specific to pediatrics that are addressed in the following list II. The
practitioner may need to change the order of examination and may not be able to perform the
entire examination in one visit III. Note that any discrepancies between the history and physical
findings should alert the examiner to the possibility of neglect/abuse and should be investigated
further IV. The examination begins when the practitioner enters the room; during the “warming
up” period the practitioner can assess the child’s behavioral patterns and interaction with the
caregiver and surroundings

A. Assess the overall health status, general symmetry of movement,

speech patterns, and nutritional status (see Tables 2-1 and 2-2) B. Note
the child’s attention to sounds and sights and overall curiosity about
the environment C. Observe the child for unusual characteristics that
might indicate genetic abnormalities
D. Focus on normal healthy body parts and perform traumatic
procedures last (e.g., EENT, genitalia, painful areas) E. Plot height,
weight, and head circumference (when appropriate) on a standardized
chart at each visit or more often if an abnormality is noted (see Table 2-
2)
1. Use the same chart at each visit for consistency and to easily monitor
growth progress 2. Measure the head circumference above the
eyebrows, above the pinnae, and over the occipital prominence 3. Use
the same weight scale (if possible) at each visit; if weighing an infant,
remove all clothes except for the diaper (weigh the diaper and subtract
the diaper weight when entering the weight in the chart)
F. Always obtain TPR (BP for children >3 years of age) at each visit (Table
2-3)
1. Monitor vital signs for deviations from normal on the chart
2. These should be plotted on standardized charts for easier evaluation
Table 2-2
Stages of Growth and Development

Age Normal Growth Rate Special Considerations

61
 Birth-12 Birth length: 9-11 in/yr Rapid, highly variable rate of growth; “catch up” and “catch
down” growth
mos Birth weight doubles by 6 mos,
triples by 12 mos, quadruples by 24 Refer if height or weight falls >2 standard deviations on growth
mos chart within 2 mos Nutritional factors should be monitored
closely
Average weight gain is 4.4-6 lbs/yr
until puberty Observe for failure to thrive for any reason
Infants should be weighed and measured at every visit
(minimum twice yearly) and more often if deviation is noted

12-36 mos Height: 3-5 in/yr Growth rate declines from the neonatal period
Average weight gain is Between 18 and 24 mos, the growth “channel” (percentile on
approximately 5 lbs/year from 2 yrs growth chart) is established Growth patterns and velocity
to adolescence established by 36 mos
Weight and measurements should be performed at least once a
year

3 yrs to Height: 2-2.5 in/yr Can calculate “mid-parental height” to establish the baseline for
puberty Weight gain: approximately 5 lbs/yr height potential. This is only an estimate: add the mother’s and
father’s heights, then add 5 in for boys or subtract 5 in for girls,
and then divide by 2
Linear growth stabilizes; changes in growth velocity signal
potential growth or health disorder Weight and measurements
should be performed at least once a year

Adolescence Growth rate is rapid and highly
variable
Onset of pubertal growth spurt:
average age is 10 yrs for girls and
12.5 yrs for boys Weight gain is
approximately 5-10 lbs/yr
Refer precocious puberty (occurring before 8 yrs of age)
Menarche occurs about 2 yrs after breast buds appear
Girls must weigh at least 88-90 lbs before menarche will occur
Once puberty begins, growth plates start to close, which
stabilizes height
Refer if puberty is delayed beyond 15 yrs of age for boys and
girls

Table 2-3
Vital Signs: Approximate Normal Findings

Age RR HR BP
0-2 mos 30-60 80-170 70-92/52-65
2-12 mos 20-30 80-150 91-109/53-67
1-3 yrs 25-35 80-150 95-105/56-68
3-5 yrs 22-32 70-120 99-110/55-70
5-11 yrs 20-30 70-110 97-118/60-76
12-18 yrs 16-22 65-105 110-130/65-85
18+ yrs 10-25 60-90 113-136/65-84
BP, Blood pressure; HR, heart rate; RR, respiratory rate.

Physical examination
I. The integumentary system is evaluated primarily with clinical inspection

A. Vascular variations in color, including cyanosis or a ruborous color of

the extremity(s) B. Characteristic rashes of possible communicable

62
 diseases
C. Ecchymosis, petechiae
D. Lesions such as moles, nevi, milia, or warts
E. Marks or discolorations suggestive of abuse occur on areas of body not
likely to be bruised (e.g., neck, inner arms, upper inner thighs), and
may be identified by the presence of patterned bruises (e.g., paddle or
hand print), numerous scars, and a history of multiple fractures,
especially of long bones F. Birthmarks, color changes with position, or
variations in skin color (e.g., vitiligo or tinea versicolor) G. Skin
plasticity, sensation, turgor, and any unusual odors
H. Eczematous changes
I. Palmar creases and hair whorls
J. Hair, fingernails, and toenails for discolorations; unusual growth
patterns, and any interdigital excoriations K. Not to be missed
1. Cyanosis, pallor, and erythema
2. Viral rash, impetigo, and dermatitis
3. Unusual patterned bruising or fractures in non–weight-bearing
infants/children, which could indicate abuse 4. Unusual spots, stains,
nevi, or supernumerary nipples
5. Jaundice
6. Umbilicated papular lesions or vesicular lesions (consider molluscum
contagiosum or herpes virus)
II. HEENT

A. The head should be observed for overall symmetry and placement of

facial parts, especially ears; inspect for scaling/crusting, dilated scalp
veins B. Observe and palpate for overriding suture lines or softening of
the occipital/parietal bones (craniotabes); this may be normal up to 4
months of age C. Palpation of fontanelles
1. More accurate if the infant is quiet
2. Posterior fontanelle closes by 8 weeks
3. Anterior fontanelle closes by 18 months
4. May palpate a slight pulsation in a normal infant

63
D. Eyes may be better visualized in dim light, as this will encourage the
infant to open eyes and look around
1. At 2 to 4 weeks, an infant should be able to follow light
2. At 3 to 4 months, an infant should have coordinated eye movement
3. Note abnormal appearance of pupils
4. Note tearing, redness of sclera or tear ducts, and any plugging of tear
ducts 5. Note presence or absence of corneal light reflex (test for
strabismus, an ocular muscle tone imbalance that can lead to blindness
if not corrected) 6. Note presence or absence of red reflex (abnormal
reflex could indicate cataracts or intraocular lesions) 7. Assess vision or
the ability to see and grasp objects without difficulty
a) visual acuity at birth: 20/200
b) visual acuity at 6 months of age: 20/100
c) visual acuity at 1 year of age: 20/50
d) visual acuity at 18 months of age: 20/20
e) vision testing charts are available for use in young patients, including
Allen picture cards, “E” chart, Sheridan-Gardiner geometric designs,
and Snellen charts
8. Perform the cover-uncover test and test EOMs
9. Perform fundoscopic examination, if possible; observe the macula,
optic disc, and retinal background and veins/arteries
E. Ears
1. Ears should be evaluated for size, shape, and placement on the head
2. Ears are considered low set if they are below a line drawn from the
lateral angle of the eye to the external occipital protuberance (Figure 2-
2). This is often associated with urinary tract disorders and mental
retardation.
3. The ear canal and TM should be evaluated. To best visualize the TM,
use the following techniques:
a) for infants: pull the auricle backward and downward
b) for older children: pull the auricle backward and upward
4. Observe the TM for mobility, color, and intactness; evaluate for wax or

64
 foreign objects 5. Hearing should be assessed at birth via auditory
brain stem testing (usually done before discharge from hospital);
question the caregiver about the test results; hearing can be tested in
the office by making a loud, unexpected noise or ringing a bell and
observing for a startle reflex; absence of the startle reflex may indicate
hearing deficits 6. Refer a school-age child without a physical reason
for failure to hear any frequency ≥25 dB on an audiometer or if the
parent or teachers identify problems. Ask the parent if the TV must be
very loud for the child to hear or if there are problems with discipline
(this can indicate hearing deficit).
7. Language skills correspond to hearing abilities
8. Infants localize sounds by 6 to 8 months of age, know several words by
12 months of age, and can articulate short sentences by 2 years of age
(see Table 2-1) 9. Speech and sound development:
a) 3 years (p, m, h, n)
b) 4 years (k, g, d, f, y)
c) 5 to 6 years (t, ng, r, l)
d) 7 to 8 years (s, ch, sh, z, j, v, zh)
F. Nose should be examined for occlusion or discharge, especially
unilateral nasal discharge
1. Observe for flaring and distress
2. Observe the nasal septum and the color of the nasal mucosa (e.g.,
bogginess, polyps) 3. Palpate the sinus areas: frontal, maxillary,
ethmoid, and sphenoid
a) maxillary and ethmoid sinus cavities are present at birth but very
small
b) the frontal sinus develops between 2 and 4 years of age but is rarely a
site of infection until 6 to 10 years of age c) the sphenoid sinus is rarely
a site of infection until 5 to 8 years of age
G. Mouth
1. Examine the lips and buccal mucosa for lesions, moistness, and
fissures; check the hard and soft palates for intactness, any unusual
nodules, and clefting 2. Evaluate the tongue for appearance,

65
 movement, and color; if possible, observe the infant sucking on a bottle
or breast for the strength of the suck reflex 3. Evaluate teeth (see Figure
2-1) for number and condition; ask about eruption history 4.
Appearance or absence of tonsils, tonsil size, color, and color of
exudate 5. Oropharynx examination of a toddler
a) have the infant/child sit with his/her back against the caregiver’s chest,
facing the practitioner, and ask the caregiver to give the infant/child a
big “hug,” encircling the upper torso and arms with the caregiver’s
arm; have the caregiver use the other arm to hold the forehead, which
will secure the head fairly well for tongue blade examination b) the
infant/child will usually open his or her mouth to “scream” and the
practitioner can get a very good look during this time and do any
swabs that are needed; gag reflexes can also be evaluated at this time
H. Not to be missed
1. Abnormal facies, paralysis, or abnormal facial expressions (consider
congenital abnormality)
2. Abnormally shaped skull or craniotabes after 4 months (consider birth
trauma, rickets, or syphilis) 3. Sunken fontanelle, dry tear ducts, and
no wet diapers (consider dehydration) 4. Nystagmus, strabismus,
amblyopia, presence of cloudy pupils (consider blindness, ocular
muscle deformity, or cataracts) 5. Loss of red reflex and light reflex
6. Unresponsiveness to surrounding noises; lacking speech (consider
deafness) 7. Nasal obstructions, snoring, or unilateral orifice discharge
8. Dental malocclusions, cavities, or missing teeth
I. Neck/lymph nodes
1. Have the child move his or her neck in all ranges of motion to
determine any limitations or pain 2. Inspect and palpate all neck
muscles for symmetry and observe any abnormal positioning of the
head secondary to a spasm (e.g., torticollis) 3. Inspect tracheal position
and palpate the thyroid and any cysts or lymph nodes in the neck 4.
Palpate the lymph nodes (see Figure 1-3 for lymph node placement)
for size, mobility, and consistency 5. Lymph nodes enlarge more often
in children than adults because of infection above the site of the lymph
node; this should resolve with warm moist compresses and antibiotics
6. Not to be missed

66
 a) a single persistent enlarged lymph node (consider cancer/lymphoma)
b) an enlarged thyroid
c) nuchal rigidity (consider infection or cervical trauma)
III. Respiratory system

A. Inspect the chest wall for shape, size, supernumerary nipples, or

unusual markings B. The chest is usually rounded until the child is
older; if an older child continues to have a rounded chest wall, suspect
an underlying pulmonary disease (e.g., cystic fibrosis) C. The shape of
the chest is usually symmetrical
1. Asymmetrical abnormalities include pectus excavatum (funnel chest)
and pectus carinatum (bird chest) 2. Sternal nodules may signal
vitamin D deficiency (rickets)
3. Observe respiratory rate, use of accessory muscles (e.g., retractions),
and pattern of breathing
a) infants are abdominal “breathers” (lungs do not fully mature until
about 8 years of age) b) infants may have periods of apnea of up to 15
seconds
D. Auscultate all lung fields (see Figure 1-4) for equal breath sounds,
abnormal breath sounds, and upper airway extraneous noises E.
Infants are obligatory nasal breathers until about 6 months of age;
nares and adenoids may swell because of allergies or exposure to
smoke. Ask about snoring and unilateral nasal discharge.
F. Nasal sounds can be heard throughout the lung fields in infants, but
are usually louder in the upper lobes because of the size of the infant
and the proximity of the bronchial tree to the chest wall G. Not to be
missed
1. Persistent wheezing/coughing or fever (consider pneumonia or
asthma)
2. Inability to clear secretions, failure to thrive, or unusual postures to
assist breathing (consider cystic fibrosis or pulmonary fibrosis)
IV. Cardiovascular system

A. Observe the child’s activity level and ask about response to exercise;
observe for any posture during activity and skin color at rest and
during activity while in the examination room B. Auscultation for the

67
 rhythm, rate, and location of heart sounds (see Figure 1-5)
1. S3: caused by turbulence of rapid left ventricle filling; it may be normal
in children and is heard at the apex or along the lower left sternal
border 2. S4: abnormal and indicates decreased ventricular compliance
(e.g., HF)
C. Murmurs (see Table 8-1) should be identified in relation to the
intensity, location, and radiation of sounds D. All new murmurs
should be initially evaluated by a pediatric cardiologist
E. All murmurs greater than grade 3/6 should be followed annually by a
pediatric cardiologist and/or echo F. Palpate pulses (see Figure 1-6) for
strength, quality, and symmetry in the bilateral upper and lower
extremities G. Palpation of PMI
1. Best felt: at the fourth intercostal space in a child <7 years of age; at the
fifth intercostal space in a child >7 years of age 2. Lower PMI may
indicate cardiac enlargement
3. Bounding PMI may indicate anemia, fever, or fear
H. Not to be missed
1. Unusual posture during activity, decrease in stamina, and/or any
pathological murmurs (congenital heart defects) 2. Poor growth or
feeding, fever, excessive sweating, or cardiomegaly (consider anemia,
myocarditis, or HF) 3. Delayed or absent femoral pulses
a) may have pulse differences between arms and legs, with pinker upper
extremities and more cyanotic lower extremities b) measure BP in both
arms and legs; if the pressure in arms is >20 mmHg over that in legs,
consider coarctation of the aorta (CoA)
V. Abdominal system

A. Observe for any peristaltic waves (as caused by pyloric stenosis)

B. Inspect shape, muscular integrity, umbilicus, and any unusual skin
markings
1. Vascular skin markings (e.g., hemangiomas) are common but
prominent veins over the abdominal wall may indicate chronic liver or
renal disease 2. The shape is usually rounded and protuberant in
infants; this slowly resolves, becoming more scaphoid with age and
mobility 3. Diastasis recti is common and can be elicited in infants

68
 when sitting up; it is not noticeable when lying flat. This usually
resolves with age and surgery is only considered if a hernia should
develop.
4. Observe the umbilicus for any hernias or exudates
a) hernias are not uncommon in infants, toddlers, and young children;
can be elicited by having the child tense abdominal muscles or raise
his or her head off the bed; usually resolve without treatment b) the
umbilical cord usually separates by 1 week after birth; if still present
after 3 weeks, suspect infection, immunodeficiency, or congenital
malformations c) exudates from the umbilicus may be caused by a
foreign object in a preschool child; clean the area well and inspect for
debris
C. Auscultate for bowel sounds and bruits
1. Bowel sounds can be referred across the abdomen in infants/children;
listen for 30 to 60 seconds if no sounds are heard initially
a) absent bowel sounds may be due to peritonitis or appendicitis
b) high pitched, tinkling sounds may be due to obstruction
2. Listen over the aorta and other large abdominal vessels (bruits are
usually easier to hear because of less abdominal fat occluding sounds)
D. Palpate the abdomen with the child’s hand over the practitioner’s and
have the child press down on your hand; this gives the child some
control over the examination and will decrease “ticklishness”
1. Palpate all quadrants (see Figure 10-1) both lightly and deeply for
tenderness, rebound, and guarding; check the liver, kidney, and spleen
for size
a) in infants and younger children, the liver may be felt 1 to 3 cm below
the rib edges; in older children, the liver should not be felt below the
rib edges b) palpate the spleen with the child lying on the right side
with knees drawn up; palpate just under the intercostal margin while
the child is taking a deep breath; if you suspect splenomegaly or injury,
DO NOT PALPATE
2. An easy way to test for rebound or guarding pain is to have the child
“blow up their belly” to touch your hand 3. Not to be missed
a) projectile vomiting (consider pyloric stenosis)

69
 b) painless abdominal mass, hematuria (consider Wilms’ tumor)
c) rigid abdomen with pain, unusual bulging noted with or without pain,
drainage from the umbilicus, or a fissure in the umbilicus (consider
hernia or cancer)
VI. Genitourinary system

A. Take a “matter-of-fact” approach to the examination

B. Observe the placement of nipples (wide spread nipples may be
indicative of genetic anomalies [e.g., Turner’s syndrome]); observe for
normal development of the breast tissue and note any discharge C.
Examine a boy with him in a “tailor sit” position to avoid testicular
retraction (cremasteric reflex); observe for testicle placement, urethral
position, penis size and shape, and circumcision D. Examine a girl
while she is in the “hands and knees” position or butterfly position
(supine with the plantar aspect of the feet touching and legs relaxed
outward) for hymenal injuries, imperforate hymen, extruding vaginal
masses, or labial adhesions (see Chapter 17 for treatment of labial
adhesions)
E. Assess rectal sphincter tone; note any masses, fissures, or bleeding
F. Elicit anal wink by gently stroking the perianal tissue with a finger or
sharp object; if normal, will cause visible puckering to the external anal
sphincter. Lack of response suggests defect in sensory or motor nerve
roots.
G. Assess sexual maturity using Tanner’s staging (see Box 2-1) H. Not to
be missed
1. Hematuria, hypospadias, abnormal curvature of penis (Peyronie’s
disease)
2. Early or delayed puberty
3. Breast or testicular masses
VII. Musculoskeletal system

A. Spine
1. Observe contours of the spine for scoliosis (see Chapter 17) 2. The
cervical spine should have full extension, flexion, rotation, and lateral
movements

70
a) a 10-degree flexion restriction is noted if one finger breadth is noted
between the chin and chest wall; atlantoaxial instability is a concern
(this is seen with Down’s syndrome) b) torticollis is noted with lateral
restriction and shortening of muscles forcing the head into lateral
movement
3. The thoracic/lumbar/sacral spine should have full mobility and the
child should be able to bend forward and touch his or hands on the
floor easily without bending the knees 4. Observe the overall shape,
contour, tone, and strength of the muscles in the back; there should be
equal movements bilaterally 5. Observe for sacral dimpling or tufts of
hair in the pilonidal area
6. Palpate the spine and paravertebral muscles for pain or spasm
B. Gait
1. Assess gait as the child enters the room and/or navigates the room;
watch for symmetry, ability to turn and stop, and smoothness of these
actions 2. Try to observe the toddler/child in the anatomical position
from all sides, front and back
a) abnormalities observed might include spinal deviation (see above),
limb alignment and length, limited ability to fully extend arms and
knees, abnormalities in feet b) observe for limping (see Limping Child
in Chapter 17) and when it occurs (e.g., walking, running, turning,
stopping)
C. Arms
1. Inspect all joints for swelling, redness, and pain with movement; offer
items to grasp and hold against resistance 2. Palpate all upper
extremity joints for pain and ROM (active, passive, and against
resistance)
a) test internal and external rotation of the shoulders, strength, and
reflexes b) supination and pronation of the elbow; flexion and
extension of the wrist and complete ROM of all finger joints; assess all
carpal and metacarpal bones for swelling and pain
D. Legs
1. In the standing position, observe the shape and alignment of the legs
(from hip to feet), both individually and bilaterally 2. Observe for
bilateral in-toeing (pigeon toed), which means that the foot turns

71
 inward while walking or running; can be considered a congenital
condition and usually corrects itself with growth. If this condition is
unilateral, painful, and grossly asymmetrical, referral to an orthopedist is
recommended.
E. Hips should be evaluated in regard to flexion, extension, internal and
external rotation, and abduction and adduction
1. Perform the Barlow-Ortolani test to detect hip dislocation; observe
buttock creases 2. Hip flexion should be 100 degrees; hip extension
should show the leg to be flat on bed 3. Hip internal rotation should be
about 35°; external rotation should be about 45°
4. Knees should be evaluated for full extension, with the posterior
popliteal fossa touching the bed, and flexion, with the knees flexed to
about 120 degrees 5. Evaluate for varus and valgus alignment
a) genu varum (bowlegs) can be physiologic under 2 years of age and
usually resolves with continued ambulation; is bilateral and seen with
in-toeing and waddling. The child usually appears “clumsy” when
ambulating.
b) genu valgum (knock knees) may be physiologic and will resolve by 6
years of age. If the deformity is unilateral and/or painful, refer to an
orthopedist.
6. To evaluate leg length discrepancy, have the child stand and observe
the iliac crest and gluteal folds, which should be even; if there is any
asymmetry, there may be leg length discrepancy. Referral is indicated
to an orthopedist if the discrepancy is >2 cm or if it causes pain or
difficulty with mobility.
F. Ankles/feet should be assessed for ankle ROM, soles of feet, and foot
alignment
1. Pes planus (i.e., flat feet) is common in infants/toddlers until the arch
develops in childhood with walking; this is nonpainful and associated
with pronation 2. The child may appear to be “flat footed” until about
3 years of age, when the fat pad starts to resolve
G. Not to be missed
1. Fractures or evidence of healed fractures in infants/toddlers
2. Swollen, red, and hot joints; poorly healing open wounds over bony

72
 areas (consider arthritic conditions) 3. Unusual growths on bone,
scoliosis, unexplained fractures, muscle mass atrophy, or abnormal
masses or “pits” in the spinal column (consider spinal cord anomalies)
4. Abnormal gait and/or pain in the hip joints, unusual protuberance
over the joints (consider hip dysplasia, cancer, or cerebral palsy) 5.
Delayed growth and development
6. Ataxia, muscle atrophy, and abnormal reflexes (consider cerebral
palsy)
VIII. Neurological system

A. The practitioner should make observations related to mobility, facial

expressions, and overall limb symmetry as well as any gait
disturbances and abnormalities in balance, coordination, and
neuromuscular development B. Skull examination
1. Size (e.g., microcephaly, macrocephaly), shape (e.g., rounded or
flattened), appearance of cranial suture lines (e.g., craniosynostosis) 2.
Fontanelles (e.g., flattened or bulging)
3. Prominence of scalp veins (increased intracranial pressure [ICP])
C. Cranial nerves
1. CN I: Olfactory sense appears at about 5 to 7 months of age
2. CN II, III, IV, VI: Optic nerves
a) fundoscopic for optic disc, macula, and veins; evaluate pupil size and
pupillary response to light (PERRLA) b) test peripheral vision by
having the child focus on his or her parent and then bring the object
into the visual range from the side and evaluate when the child turns
his or her head c) monitor for nystagmus at rest and with EOM
d) blink reflex is not strong at birth and starts to develop at about 3 to 4
months and is fully developed by 12 months
3. CN V: test sensation of face; chewing or sucking strength and corneal
reflex 4. CN VII: observe for facial symmetry and sucking or taking in
foods; taste is more difficult in younger children because they do not
understand different tastes but may relate to “good” or “bad” taste 5.
CN VIII: check hearing by making a loud noise and watching for a
reaction; older children may be tested with whispering and having
them tell you what was whispered 6. CN IX, X: gag reflex can be

73
 checked when examining the throat; CN X controls uvula and palate
movement (the uvula will deviate to the unaffected side if there is
vagal nerve dysfunction) 7. CN XI: watch for symmetry in turning
head and check turning against resistance to evaluate the strength of
the sternocleidomastoid muscle 8. CN XII: tongue movement can be
evaluated by watching the tongue and evaluating sucking strength
D. Motor examination
1. Watching a toddler/child walk or run assists in evaluation of cerebellar
function for balance and coordination; testing passive ROM evaluates
motor strength and identifies any abnormalities of tone 2. Test
pronator drift by having the child extend his or her arms with eyes
open and palms up, then have the child close his or her eyes and watch
the extended arms for drifting. Try to press down on the arms while
extended; this is a good test for assessing strength in the upper
extremities.
3. Test proprioception with Romberg’s test: have the child stand with
eyes closed and evaluate the child’s ability to stand without
swaying/falling
E. Sensory examination distinguishes between different levels of touch,
vibration, and position; test higher function by asking the child to note
objects (that would be familiar to his or her age) through touch with
eyes closed
F. Reflexes should be tested from birth according to age (Table 2-4); after
5 years of age, reflexes should be the same as in adults G. Observe for
cutaneous abnormalities, dimples, vascular malformations, and tufts of
hair over the lower back H. Refer to the Denver Developmental
Screening Tool, Denver Articulation Screening Exam, and Dubowitz
Scale for further testing of speech and cognition
I. Not to be missed
1. Hydrocephaly, macrocephaly, microcephaly
2. Headaches (benign intracranial hypertension)
3. Uncontrolled, inconsolable crying (consider increased intracranial
pressure) 4. Seizure (consider trauma or disease process)
5. Loss of use of extremities, abnormal mass or pitting in the spinal
column (consider neural tube deformity)

74
 FIGURE 2-2 ​Normal and Low-Set Ears. Source: (From James, S.R., Nelson, K.A.,
& Ashwill, J.W. [2007]. Nursing Care of Children: Principles and Practice. Philadelphia:
Elsevier.)

Table 2-4
Normal Primitive Reflexes

Reflex Definition Disappears by Age

Rooting When the cheek is stroked, the head turns toward the 3-4 mos
stimulus.
Tests tactile reflexes and proprioception

75
 Moro With sudden movement of the body from the neutral 6 mos
position to the lower position, arms flail outward and
are then brought into body; hands will open and the
infant will usually cry out.
Tests general level of excitability
Palmar Flexion of fingers, fisting when an object is placed in an 3-5 mos
grasp
open hand
Considered abnormal if the response is asymmetrical or
is absent before 2-3 mos
Tests tactile reflexes and proprioception
Tonic When the head is turned to the side while the rest of the 6-7 mos
neck body lies flat on table. Normal response is extension of
reflex the arm and leg on the side that the head is turned and
(fencer’s flexion of the opposite arm and leg.
position)
Considered abnormal if the response is not symmetrical
Tests auditory, visual, and vestibular reflexes and
proprioception
Parachute The infant is suspended horizontally with the face 8-9 mos
response down and is quickly brought down toward the floor
(make sure that the infant is held securely). Normal
response is arms extended and hands open.
Tests symmetry of movement
Stepping 4-5 mos
Stepping occurs when the sole of the foot is placed on
response the table; infant appears to be walking.
Babinski’s Positive sign is dorsiflexion of the great toe and fanning Can be normal until 1 yr
sign of other toes after firm stroking of the plantar aspect of of age; usually
the foot. disappears by the time
the toddler starts
Abnormal if asymmetrical response walking.
Tests pyramidal tract dysfunction
Clonus Maintaining dorsiflexion of the foot after stimulation or
having sustained clonus after checking reflexes is
ALWAYS abnormal

Child abuse

I. Definition: nonaccidental, purposeful physical, emotional, or sexual abuse directed at a minor

child II. Physical abuse is defined as nonaccidental trauma and is usually committed by family
members, caretakers, or other people in the family setting; occurs in daycare settings; also seen
with “bullying” in school settings III. A high level of suspicion is needed to recognize risk factors
that contribute to child abuse. This is of utmost importance for the practitioner as this may be the

76
child’s first entry into the health care system.

A. Risk factors identified in the family setting that contribute to abuse

may include the following:
1. Number of children in household under 3 years of age (infants are at
the highest risk because of complete reliance on the caregiver for all
physical needs) 2. Family patterns of violence
3. Poverty or very low socioeconomic status
4. Lack of parenting skills due to immaturity and poor coping skills
5. Lack of extended family support
6. Single-parent status and social isolation
7. Financial difficulties
8. Drug or alcohol abuse or overuse
B. Risk factors associated with the child’s physical abilities
1. Mental or developmental delays/disability resulting in different
physical appearance from peers 2. Hearing or visual difficulty of any
degree of severity (e.g., wearing hearing aids or glasses) 3. Small size
without developmental delays
4. Immunodeficiency diseases (e.g., AIDS) or musculoskeletal disorders
(e.g., cerebral palsy)
C. Risk factors related to physical settings other than the home
1. Large daycare, preschool, or primary school settings with poor
monitoring systems for intervention in cases of physical violence 2.
Multiple family settings
3. Having a distance to walk home after school (e.g., either in urban or
rural settings) 4. Frequent stays in shelters
IV. Types of abuse vary from minor to major, with some leading to death

A. Neglect of basic needs or education or abandonment by the caregiver

B. Emotional abuse involves caregiver’s detachment from the child’s
needs; unrealistic expectations and angry outbursts over insignificant
actions/issues
V. Child behaviors indicative of emotional abuse

A. Withdraws from physical touch or exhibits aggressive behaviors if

77
 approached by the caregiver or others in the family; may exhibit same
behaviors with noncaregivers in other settings B. May “cling” to the
caregiver and exhibit terror if separated from the caregiver (this is not
as bothersome if the child is 6 to 18 months of age and exhibits
“stranger separation”) C. Somatic complaints of soreness while
moving without obvious bruising
D. Wears inappropriate clothing for the weather
VI. Caregiver behaviors indicative of emotional abuse of the child

A. Yelling at inappropriate times and more often than necessary

B. Refusing to touch or look at the child when needed
C. Verbally belittling, shaming, ridiculing, or threatening the child
VII. Suspect physical abuse in case of the following:

A. Repeated visits to a health care facility for injuries that do not coincide
with the provided stories or there are questionable causes for injury or
condition B. Any injuries that occur in non–high-impact areas of the
body, such as the face, head (especially sides), chest, genital area,
buttocks, upper arms, or thighs C. Any patterned marks (e.g., hands,
buckles, broom handles), especially if the child names the object D.
Soft tissue injuries such as burns, bruising, lacerations, or bite marks,
especially if the story does not fit with the injury (e.g., water burns
from pulling hot water off the stove should involve the chest and
abdomen, not feet or buttocks) E. Multiple fractures in the rib area,
fractures in various stages of healing, or femur fractures in a
nonambulatory infant
VIII. Sexual abuse

A. Defined as any adult in a position to force or coerce a child into

unwanted sexual activity, which could be touching, forcible
penetration into orifices, or pornography; is usually more subtle and
the child may present with the following:
1. Complaints of dysuria or pain in the genital area
2. Vaginal discharge, bleeding, itching, or swelling
3. Rectal pain with or without itching
4. Acting out sexually in inappropriate ways
B. If sexual abuse is suspected, the child should be interviewed by a

78
forensic interviewer and practitioner to ensure adequate
documentation C. ALL health care providers are mandated reporters and are
obligated to notify authorities or HOT-LINE for child sexual/physical abuse
D. If the practitioner is concerned for the child’s welfare, the
authorities should be notified immediately and the child can be sent to
the hospital for his or her protection

79
CHAPTER 3

80
Geriatric assessment
Introduction

I. The goal is maintaining and enhancing the daily functioning of the elderly patient; normal
changes of aging are often complicated by chronic and/or acute illnesses II. With comprehensive
assessment, in addition to physical examination, many parameters of health are reviewed,
including the following:

A. Nutrition
B. Gait and balance; ability to perform ADLs
C. Visual and auditory perception
D. Social and psychologic assessment
III. The clinical presentation of a health problem in an elderly patient often appears in an atypical
manner and may mimic many different illnesses IV. Because of the limited time in a primary care
setting, the assessment tools presented in this chapter can be conducted within a few minutes
and have been documented in terms of their validity and reliability

A. Functional status of decline, which often has a subtle onset and

progression, can be identified B. With early identification of the
problem, early intervention(s) may ameliorate the condition or slow its
progress

P r a c t i c e Pe a r l s f o r A s s e s s m e n t

• Use the patient’s last name when addressing him or her (unless the patient requests
otherwise).
• Sit level with the patient during the interview.
• Make sure the room is well lit; do not stand in front of a bright light or window.
• Minimize background noise as much as possible.
• Note reliability of the health history information.

81
Health history*
I. Chief complaint

A. Complaints may be numerous

B. Help patients identify which complaint is personally of greatest
concern to them
II. History of present illness (HPI)
III. Self-rated health (elderly patients often see themselves as healthier than practitioners do) IV.
Past medical history

A. Ask the patient specifically about reported illnesses and which

provider gave that diagnosis; do not accept a diagnosis B. Ask about
past blood transfusions
C. Medication history is extremely important (including pain
medications, laxatives, eye medicines, OTC sleep aids, and cold or
allergy medicines); it is advantageous to have patients bring all of their
current OTC medications and prescriptions in their bottles at the time
of the visit
V. Patient profile

A. Marital status and relationship with spouse

B. Children (e.g., relationship and frequency of contact with them; obtain
their telephone numbers if patient wants you to share information
with them. Be sure that the patient has signed the HIPAA form
allowing information to be shared).
C. Living arrangements
1. With whom?
2. Where (e.g., an apartment or home, assisted living facility)?
3. What type of heating and cooling system is used at home?
D. Support systems (e.g., family, friends, community services) E. Recent
losses, including pets
F. Education, occupation, and retirement or current employment G.
Adequacy of finances and health insurance
H. Transportation, especially to health care facilities I. Typical daily

82
 activities (if indicated)
VI. Nutrition

A. Determine if the diet is adequate and if the patient is at risk for

malnutrition. Consider asking about the previous day’s food intake;
has the patient’s weight been stable?
B. Conditions associated with malnutrition include chronic alcoholism,
chronic myocardial or pulmonary diseases, cognitive disorders or
depression, malabsorption syndromes, and polypharmacy
VII. Sleep patterns

A. What time does the patient go to bed and get up?

B. How often does he or she wake at night and for how long? What
wakes them?
C. Is the sleep restful?
VIII. Safety

A. See Functional Assessment at the end of this chapter.

B. Does the patient have concerns about possible abuse or neglect?

83
Comprehensive geriatric assessment
Note: If there are discrepancies between the history answers and physical findings, consider hidden
problems such as falls or abuse.

Integumentary system
I. See Table 3-1 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. What changes have you noted in your skin’s condition over the last
few years?
B. Has there been any delayed wound healing?
C. Have you had any new or changing skin lesions, itching, or pain?
D. Do you have a history of DM or PVD?
E. Have you received the shingles vaccine (Zostavax)?
Table 3-1
Physiologic Changes and Abnormal Findings: Integumentary System

Physiologic
Clinical Correlation Points Not to be Missed
Changes
Loss of elasticity Wrinkles Abnormal skin lesions (e.g., actinic keratosis, skin
cancers)

Loss of elastin, Paper-thin skin prone to breakdown and Dehydration

collagen, sub-q fat injury
Hypothermia
Decreased sweat and Dry skin and pruritus Pruritus due to renal or hepatic disease, DM,
oil glands Difficulty in regulating body temperature, hyperthyroidism, drug allergy, iron deficiency
especially with changes in environmental anemia, parasitic infections Heat stroke
temperatures

Increased vascular Senile purpura Bruising, purpura, or abrasions secondary to falls or

fragility abuse

Slower epidermal Slower wound healing

growth rate

Hair turns gray or Potential effect on self-esteem

white and feels thin
and fine

Hair distribution “Male pattern” baldness Localized hair loss due to PVD
changes
Decreased axillary and pubic hair Diffuse alopecia due to hypothyroidism, iron
Women may develop bristly facial hair deficiency, hypoproteinemia
and/or have hair thinning in the frontal
and vertex areas of the scalp

Nails grow more Nails prone to splitting Nails that are thickened or overgrown, causing pain
slowly and develop with shoes or with walking

84
 longitudinal ridges

P r a c t i c e Pe a r l s f o r I n t e g u m e n t a r y S y s t e m

• Elderly patients are at a higher risk of ulcer formation because of decreased turgor and
subcutaneous fat.
• With skin changes, remember to ask about a history of allergies or atopy, work history, and
environmental exposure (including sun).
• The incidence of herpes zoster peaks in people aged 50 to 70 years, and postherpetic
neuralgia occurs more frequently in people aged >70 years.
• Current recommendations for zoster (shingles) vaccine: once for all people aged ≥60 years; if
also administering a pneumococcal vaccine, separate the two injections by at least 4 weeks.
• Signs of neglect can include poor grooming and bedsores.

Sensory system

I. See Table 3-2 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. Do you have any difficulty climbing steps or driving?

B. When was your last driving test and where do you drive; or if the
patient does not drive, who drives for him or her?
C. When were you last tested for glaucoma? If you have glaucoma, how
do you manage the eye drops?
D. Do you have any problem with night vision?
E. Do your eyes feel dry or burning? How do you manage this?
F. Have you noticed a change in your hearing or taste?
G. Have you noticed any burns, bruises, or cuts that you do not know
how they occurred?
Table 3-2
Physiologic Changes and Abnormal Findings: Sensory System

Physiologic
Clinical Correlation Points Not to be Missed
Changes
Eye skin loses Wrinkling and drooping (may cause
elasticity decreased vision or visual defects) May

85
 have ectropion or entropion

Distorted depth Incorrect assessment of height of curbs Falls due to other conditions (e.g., stroke or
perception and steps arrhythmia)
Changes in retina, Decreased visual acuity Macular degeneration
choroid, and skin Visual fields narrow DM
Slower light-to-dark adaptation (patient
needs more light to see)

Increased intraocular Increased incidence of glaucoma Glaucoma

pressures

Lens turns yellow Decreased visual acuity (may affect safe Cataract
and loses elasticity driving)
Color vision may be impaired (blue, green,
violet)

Decreased tear Dry or burning eyes

production

Cilia in ear canal May cause cerumen build-up Impaired hearing due to cerumen impaction
become coarse and Harder to hear consonants and to localize Social isolation due to hearing loss
stiff sound Hearing loss due to Paget’s disease, ototoxic
Gradual Difficulty hearing whispered words or in a medications, vascular or mass lesions; if no obvious
sensorineural noisy background cause for loss of hearing, refer to ENT
hearing loss, starting
in the 50s

Decreased number May have decreased sense of smell (which Potential hazard if the patient cannot detect harmful
of olfactory nerve may affect appetite, leading to possible odors
fibers weight loss) If acute loss of smell, consider tumor

Altered taste Possible weight loss or gain Zinc deficiency

sensation May have edema due to increased salt Medications that may affect taste
intake DM neuropathy

Reduced tactile Decreased ability to sense pressure, pain, Vascular diseases

sensation and temperature DM
Neurological disorder
Burns

P r a c t i c e Pe a r l s f o r S e n s o r y S y s t e m

• The degree of pain in elderly patients may not accurately reflect the seriousness of the
underlying condition.
• Blue or yellow nightlights are safer than white ones (less glare).

Respiratory system

86
I. See Table 3-3 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. Do you have any SOB or fatigue with your normal activities?

B. What is your usual level of physical activity?
C. Do you use O2: at night, with activity, or all the time?
D. For patients with COPD: How are you getting along each day? Has
your weight changed? When was your last respiratory infection and
hospitalization?
E. Have you received pneumonia vaccines?
F. Do you get a yearly flu shot?
Table 3-3
Physiologic Changes and Abnormal Findings: Respiratory System

Physiologic
Clinical Correlation
Changes
Rib cage less mobile Commonly results in an increased
AP diameter
May obscure heart and lung sounds
Points Not to be Missed
Thorax changes due to COPD
Decreased breath sounds due to effusion, atelectasis,
pneumonia, COPD

Decreased lung tissue Decreased vital capacity SOB or rales due to HF, COPD, or pneumonia
elasticity Increased residual volume Deconditioning

Ciliary atrophy Change in mucociliary movement Pulmonary infection

P r a c t i c e Pe a r l s f o r R e s p i r a t o r y S y s t e m

• Elderly patients may not have respiratory signs and symptoms until late in the course of a
disease (e.g., patients with pneumonia may have a decreased level of responsiveness,
confusion, poor appetite, or evidence of falls).
• Using a stethoscope with a pediatric diaphragm may be helpful for patients with prominent
ribs.
• The most common respiratory complaint is dyspnea; the cause may be cardiac, respiratory,
metabolic, mechanical, or hematologic.
• Rales (or crackles) are the most common physical finding; the cause may be age-related
fibrotic changes, infection, or cardiac or pulmonary disorders.
• Current recommendations for pneumonia vaccine:

• Pneumovax 23: for all people aged >65 years and for those aged <65

87
 years if immunocompromised or with a chronic disease (e.g., lung,
cardiovascular, liver, renal); vaccination should be repeated once after
5 years if the patient was <65 years of age at first vaccination, has
chronic renal failure, or is immunocompromised.
• Prevnar 13: given ≥12 months after Pneumovax 23.
• If Prevnar 13 is given first, Pneumovax 23 can be given 6 to 12 months
later.

Cardiovascular system

I. See Table 3-4 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. Do you get dyspneic with activity? Is it increasing?

B. Do you ever experience edema?
C. Have you ever experienced dizziness or syncope?
D. If you have HF, how often do you use OTC NSAID medicines such as
ibuprofen?
Table 3-4
Physiologic Changes and Abnormal Findings: Cardiovascular System

Physiologic Changes Clinical Correlation Points Not to be Missed

Atherosclerosis and Increased incidence of HTN and HTN secondary to anemia or
arteriosclerosis CHD hyperthyroidism
Pedal pulses may be difficult to Changes indicating PVD
palpate Aneurysms

Decreased compliance S4 may be audible Increased fatigue or exercise

of left ventricle intolerance

Decreased sensitivity of Valsalva maneuver may cause a Falls secondary to postural

baroreceptors sudden drop in BP hypotension
Volume depletion
Postural hypotension secondary
to the use of medication

ECG changes may ECG changes secondary to

include the following: ischemia, injury, or infarction
Decreased precordial (see Table 8-5)
QRS voltage
ST and T wave changes

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 Prolonged PR and QT
intervals (QRS
remains normal)
Ectopic (extra)
heartbeats

Heart valves thicken Increased incidence of murmurs, Pathologic murmur (see Table
especially aortic stenosis and mitral 8-1)
regurgitation

Decreased number of Slower or irregular heart rate Atrial fibrillation

pacemaker cells
“Physiologic changes” are so interrelated with lifestyle changes that it is difficult to determine which are truly physiologic changes.

P r a c t i c e Pe a r l s f o r C a r d i o va s c u l a r S y s t e m

• Systolic murmurs are common in elderly people and frequently indicate aortic stenosis.
• Although S4 can be normal or with HTN, S3 warrants investigation for other signs of HF.

• Check BP while the patient is lying, sitting, and standing to evaluate for orthostatic
hypotension; wait 2 minutes between position changes to allow baroreceptors to
compensate; evaluate further if systolic BP drops ≥20 mmHg and/or diastolic BP drops ≥10
mmHg.
• Chest pain is not always present with severe disease or even with MI.
• Edema may be caused by HF, protein malnutrition, PVD, venous varicosities, or lymphatic
obstruction.
• Elderly patients may develop postprandial hypotension: systolic BP drops ≥20 mmHg
within 75 to 120 minutes after a meal.

Gastrointestinal system

I. See Table 3-5 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. Have you lost any teeth? Do you have partial plate(s) or dentures?
B. Are you able to care for your teeth or dentures?
C. Can you chew all types of food? Do you have trouble with any foods?
D. How do you obtain groceries and prepare your meals?
E. Do you eat alone or share meals with others?

89
 F. What did you eat yesterday for meals and snacks?
G. How often do your bowels move? Do you take anything for
constipation?
Table 3-5
Physiologic Changes and Abnormal Findings: Gastrointestinal System

Physiologic Changes Clinical Correlation Points Not to be Missed

Dental enamel thins and gums Tooth and gum decay Insufficient nutrition
begin to recede Tooth loss may lead to malocclusion Periodontal disease
Poorly fitting dentures

Decreased saliva production Dry mouth Dry mouth due to medications or

Increased susceptibility to injury and systemic disease
infection Dysphagia
Decreased ability to digest foods

Delayed esophageal emptying
Occasional discomfort if food stays longer in
the esophagus
GERD or hiatal hernia
Barrett’s esophagus
Medication reaction or side effect
Dysphagia due to esophageal stricture,
tumor, or CNS dysfunction

Decreased gastric acid May delay absorption of certain vitamins and Pernicious anemia
secretion minerals (e.g., iron, calcium, vitamin B12) Gastric cancer
and medications

Decrease in liver size with May have significant effect on drug Drug toxicity: fewer albumin-binding
concomitant decrease in metabolism sites results in more “free” drug (e.g.,
albumin production digoxin, warfarin)

Decreased muscle tone and May contribute to constipation, esophageal Bowel changes due to tumors,
atrophy of mucosa spasm, diverticulosis dehydration, loss of defecation reflex

P r a c t i c e Pe a r l s f o r G a s t r o i n t e s t i n a l S y s t e m

• Abdominal pain

• Abdominal pain in elderly patients can be a vague symptom of a

serious or life-threatening disease—do not take this lightly.
• With abdominal pain, obtain an ECG to rule out MI.
• Abdominal pain associated with confusion and shoulder pain may be
observed with lower lobe pneumonia.

90
 • Because of diminished muscle mass, an elderly patient may not have a
rigid abdomen with peritoneal irritation.
• Elderly people are prone to an atonic bowel, which often leads to laxative abuse.
• Elderly patients can also have anorexia or bulimia; for a poor appetite mirtazapine
(Remeron) 7.5 to 15 mg hs, cyproheptadine (Periactin) 4 mg 2 to 3 times qd, or doxepin
(Sinequan) 25 to 50 mg qd may be tried.
• Malnutrition can be a sign of neglect.

Musculoskeletal system

I. See Table 3-6 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. Have you noticed any weakness in the past year?

B. Have you noticed an increase in falls or stumbling?
C. Do you use anything to help you get around (e.g., cane)?
D. How often and for how long do you exercise? What type of activity?
Table 3-6
Physiologic Changes and Abnormal Findings: Musculoskeletal System

Clinical
Physiologic Changes Points Not to be Missed
Correlation
Loss of muscle mass and Decreased ROM, gait Accelerated changes due to immobility
muscle strength changes Increased falls

Tendons shrink Decreased ROM Decreased ROM due to fractures, osteoporosis, inflammation, or
Gait changes contractures Falls or increased fall risk

Deterioration of joint May lead to pain and Pain due to fracture

cartilage limited movement Bursitis
Gait changes “Frozen” joint
Osteoarthritis Falls or increased fall risk

Decreased bone mass and Osteoporosis Fracture

osteoblastic activity Postural changes (e.g., Gait and posture changes
kyphosis)
Decrease in height

P r a c t i c e Pe a r l s f o r M u s c u l o s k e l e t a l S y s t e m

91
 • Inspect muscles for atrophy and bones for any deformities; muscle tone is evaluated by
passively moving each limb to feel for any rigidity.

• Increased tone: marked resistance or spasms

• Decreased tone: no or minimal resistance
• ESR and alkaline phosphatase levels rise in elderly people.
• Pain and stiffness are the most common musculoskeletal complaints in elderly people.
• A change in gait may result from deconditioning or from a musculoskeletal or neurological
cause.
• Muscle weakness is not a normal aging process; look for a cause (e.g., DM, hypokalemia, or
thiamine deficiency due to alcohol abuse).

• Evaluate by having the patient stand from sitting in a chair; if the

patient must use his or her arms, there is muscle weakness.
• Falls may be an early sign of an underlying illness.
• Fracture(s) can be a sign of abuse or of a new-onset or progressing problem with
gait/balance.

Genitourinary system

I. See Table 3-7 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. Males
1. Do you have difficulty urinating: hesitancy, weaker force of stream, or
dribbling?
2. How many times at night do you get up to urinate?
3. Do you have any urinary incontinence?
B. Females
1. Have you noticed any bleeding since menopause?
2. Do you have any vaginal itching, burning, or dryness or bleeding or
pain with intercourse?
3. Do you feel any pressure in the genital area or loss of urine with
urgency or when coughing, laughing, or sneezing?
Table 3-7
Physiologic Changes and Abnormal Findings: Genitourinary System

Physiologic
Clinical Correlation Points Not to be Missed
Changes

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 Males
Decreased testosterone Slower and less intense sexual response Impotence
levels

Decrease in the size

and firmness of
testicles

Decrease in scrotal Less rugae in scrotal skin and contents hang lower
muscle tone

Prostatic hypertrophy Urinary frequency, hesitancy, change in stream Prostate cancer

UTI due to difficulty emptying the
bladder

Females
Decreased estrogen Vaginal dryness and fragility UTI
levels
Narrowing of the vagina Incontinence
UTI symptoms without infection Palpable ovaries
Cessation of menses Postmenopausal bleeding

Decreased elasticity of Cystocele (see Practice Pearls in

pelvic ligaments Chapter 12) Uterine prolapse

Atrophy of breast Breasts become more pendulous Breast cancer

tissue

Both Sexes
Loss of glomeruli and Decreased kidney function; may need to modify eGFR less than 60 ml/h (see Chronic
reduced renal mass medication doses Kidney Disease in Chapter 12)

Reduced bladder Decreased bladder capacity may lead to increased Nocturia due to BPH, renal
muscle tone nocturia or urge to urinate only when the bladder is full insufficiency, HF, or DM

P r a c t i c e Pe a r l s f o r G e n i t o u r i n a r y S y s t e m

• With nocturia, ask when diuretics are taken and what the fluid intake is before bedtime.
• With impotence, look for a cause; it may be psychologic, physiologic, or pharmacologic.
• With decreased renal function and use of ACE inhibitors, do not use NSAIDs.
• Consider sexual abuse with signs of minor trauma to the anogenital area or STI.

Endocrine/immune systems

I. See Table 3-8 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. How often do you check your blood sugar?

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 B. Do you ever have low blood sugar spells?
C. If using an injectable medication, what difficulties (if any) do you have
with the injections and do you prepare the insulin for injections
(possible vision problems)?
D. What was your last A1c?
E. Do you have any numbness or tingling in your feet? Do you feel your
feet when you stand up?
Table 3-8
Physiologic Changes and Abnormal Findings: Endocrine/Immune Systems

Points Not to be
Physiologic Changes Clinical Correlation
Missed
Decreased hormone secretion and diminished Stresses, such as surgery or trauma, may
tissue sensitivity to hormones increase mortality

Fibrosis of thyroid gland Hypothyroidism signs and symptoms Myxedema

Decreased basal metabolic rate Increased incidence of obesity and altered DM

carbohydrate tolerance

Defects in temperature regulation Reduced sweating Infection

Fever not always present with infection

Decreased number of T cells and T cell function Delayed hypersensitivity reactions Reactivation of latent
Increased incidence of infections infections

Increased prevalence of autoimmune Autoimmune

disorders disorders

Increased IgA and decreased IgG levels Increased prevalence of infection

Decreased activity in the renin-angiotensin- Hyperkalemia

aldosterone system

P r a c t i c e Pe a r l s f o r E n d o c r i n e / I m m u n e S y s t e m s

• Atypical presenting symptoms of DM in elderly people include altered mentation, behavior

changes, sleep disturbances, incontinence, weight loss, anorexia, and falls.
• Earlier warning signs of DM may include shin spots and recurrent skin infections (especially
yeast infections).
• Any changes in eye appearance or heart rate warrant evaluation for a thyroid problem.
• Infections

94
 • The usual symptoms of infection (e.g., fever, chills, leukocytosis, and
tachycardia) may be blunted or absent in elderly patients.
• The most common atypical signs and symptoms of infection include
failure to thrive and changes in mental status, activity, appetite, or
weight.
• Pneumonia and influenza are the most common causes of death.
• Overlooked sites of infection include the lining of the heart, teeth, feet,
and GI tract.
• Encourage a yearly influenza vaccine. See Practice Pearls on page 51 for pneumococcal
vaccine recommendations.

Neurological system

I. See Table 3-9 for Physiologic Changes and Abnormal Findings II. Additional questions to ask

A. Have you noticed any dizziness (lightheadedness—not vertigo)? If so:

1. Does it seem associated with changes in position (e.g., turning over in
bed or getting up or down)?
2. Is it associated with a decrease in hearing?
B. Have you noticed any changes in memory or mental functioning?
Have you gotten lost in familiar surroundings (e.g., driving to the
grocery store or home)?
C. Have you noticed any muscle weakness or tremors?
D. Have you had any sudden vision changes (e.g., halos, lines, or colors)
or brief blindness?
Table 3-9
Physiologic Changes and Abnormal Findings: Neurological System

Physiologic Clinical
Points Not to be Missed
Changes Correlation
Loss of neurons Decreased Achilles Falls
and nerve fibers tendon reflex

Slower impulse Slower reaction time Falls or injuries (e.g., burns)

conduction and decreased Changes due to PVD, CNS disease, or neuropathies
between neurons vibratory sensation
Decreased pain
sensation

Atrophy of brain Loss of completion of Subdural hematoma

activities or memory

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 loss

Modest decline Benign loss, usually Mild cognitive impairment

in short-term involving more Dementia
memory trivial events
Delirium
Depression
Medication-related cause (see Beers list for inappropriate medications for the
elderly; can be accessed on-line) Patient unable to safely set up own
medications or remember what has been taken

Changes in the More or less time Sleep changes due to dementia, depression, medications, sleep deprivation
sleep-wake cycle sleeping
May have
nightmares

P r a c t i c e Pe a r l s f o r N e u r o l o g i c a l S y s t e m

• Because there are few significant neurological changes associated with aging, most
neurological decline is evidence of a disease process.
• Mental (cognitive) status can be evaluated during the history and examination, using the
Short Portable Mental Status Questionnaire (Box 3-1); also consider a brief screening tool for
depression (Table 3-10, Yesavage Geriatric Depression Scale). Current guidelines do not
support screening asymptomatic elderly patients for dementia.
• With changes in consciousness (e.g., confusion, lethargy), check for UTI and pneumonia.
• Sensory testing is crucial in elderly patients. Test distal arms and legs bilaterally for both
light touch and pain.
• The most common peripheral neuropathies are caused by type 2 DM, alcohol abuse
(thiamine deficiency), and vitamin B12 deficiency.
• Tremors should be evaluated.
• Dizziness may be caused by problems with the eyes or ears or with the cardiovascular,
musculoskeletal, or neurological systems.
• Gait evaluation is essential in most elderly patients (see Table 3-11 for Tinetti Balance and
Gait Evaluation).
• For insomnia, try mirtazapine (Remeron) 7.5 mg or trazodone (Desyrel) 25 mg at hs.

Box 3-1

Short Portable Mental Status Questionnaire (SPMSQ)

What is the date today (month/day/year)?
What day of the week is it?

96
 What is the name of this place?
What is your telephone number? (If no telephone, what is your street address?)
How old are you?
When were you born (month/day/year)?
Who is the current president of the United States?
Who was the president just before him?
What was your mother’s maiden name?
Subtract 3 from 20 and keep subtracting 3 from each new number all the way down.
Scoring:
0-2 errors = intact
3-4 errors = mild intellectual impairment
5-7 errors = moderate intellectual impairment
8-10 errors = severe intellectual impairment
Allow one more error if the subject had no grade school education.
Allow one fewer error if the subject had education beyond high school.
From Pfeiffer, E. (1975). A short portable mental status questionnaire for the assessment of organic brain deficit in elderly patients.
Journal of the American Geriatrics Society, 23(10), 433-441.

Table 3-10
Yesavage Geriatric Depression Scale (GDS): Short Form

Are you basically satisfied with your life? Yes/NO

Have you dropped many of your activities and interests? YES/No
Do you feel that your life is empty? YES/No
Do you often get bored? YES/No
Are you in good spirits most of the time? Yes/NO
Are you afraid that something bad is going to happen to you? YES/No
Do you feel happy most of the time? Yes/NO
Do you often feel helpless? YES/No
Do you prefer to stay at home rather than going out and doing new things? YES/No
Do you feel you have more problems with memory than most? YES/No
Do you think it is wonderful to be alive now? Yes/NO
Do you feel pretty worthless the way you are now? YES/No
Do you feel full of energy? Yes/NO
Do you feel that your situation is hopeless? YES/No
Do you think that most people are better off than you are? YES/No
Score 1 for each answer in capitals.
0-5: not depressed
6-15: depressed
From Yesavage, J.A., Brink, T.L., & Rose, T.L. (1983). Development and validation of a geriatric depression screening scale: a
preliminary report. Journal of Psychiatric Research, 17, 37-49.

97
Assessing cognitive and emotional status
I. Additional questions to ask

A. Do you have a living will or advanced directives or have you

designated a POA for health care choices?
B. Have you thought about end-of-life decisions (e.g., CPR or code
status)?
C. Do you have a will or a financial POA?
D. What gives your life meaning and value?
E. Are you part of a spiritual or religious community?
F. Do you have friends or family that you communicate with regularly?
How often and in what way (e.g., by phone, by computer, in person)?
II. Assessment tools

A. Short Portable Mental Status Questionnaire (SPMSQ) (see Box 3-1)

1. Test detects intellectual impairment in elderly people 2. Score can be
adjusted to reflect education
B. See Cognitive Impairment in Chapter 18 for assessment of mild
cognitive impairment and dementia C. Geriatric Depression Scale
(GDS) (see Table 3-10)
1. Completed by the patient directly or by interviewing the patient 2.
Short form has 15 questions; can be completed in 5 to 7 minutes

P r a c t i c e Pe a r l s f o r C o g n i t i ve a n d E m o t i o n a l S t a t u s

• Assessing the cognitive and emotional status can create anxiety for the patient; interspersing
assessment questions throughout the interview or examination can reduce stress.
• Develop a rapport with the patient before beginning assessment.
• Provide a quiet, private environment.
• Ensure that the patient has the necessary aids (e.g., glasses or a hearing aid).
• Consider abuse with an overbearing caretaker, new-onset depression-or dementia-like

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behavior, failure to pay bills, or abrupt changes in finances.

99
Functional assessment
I. Assessment tools

A. Activities of Daily Living Index Evaluation Forms

1. Valid measure of ADLs
2. Completed by the interviewer in approximately 3 to 4 minutes 3.
Helps to identify ADLs with which the patient needs assistance (e.g.,
through rehabilitative therapy, adaptive devices, or personal care
assistance)
B. The Vulnerable Elders Survey (VES) 13 Scale (see Table 3-11)
1. Can be self-administered or administered by nonmedical personnel in
<5 minutes 2. Identifies community-dwelling elders at an increased
risk of functional decline or death over a 5-year period
Table 3-11
The Vulnerable Elders Survey (VES)

Domain Score
Age: 1
75-85 yrs 3
>85 yrs
Self-rated health: 0
Good, very good, and excellent 1
Fair and poor
Activities of daily living (ADLs)/instrumental activities of daily living (IADLs):
Needs assistance with: 1
Bathing or showering 1
Shopping 1
Money management 1
Transfer 1
Light housework
Difficulty in special activities: 1
Kneeling, bending, and stooping 1
Performance of housework (e.g., scrubbing the floor) 1
Reaching out and lifting upper extremities above the shoulder 1
Lifting and carrying 10 lbs 1
Walking quarter of a mile 1
Writing or handling and grasping small objects
From Saliba, D., Elliot, M., Rubenstein, L.Z., Solomon, D.H., Young, R.T., Kamberg, C.J., & Wenger, N.S. (2001). The Vulnerable Elders
Survey: a tool for identifying vulnerable older people in the community. Journal of American Geriatric Society, 49(12), 1691-1699.
A score of ≥3 indicates a vulnerable elder.

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 P r a c t i c e Pe a r l s f o r F u n c t i o n a l A s s e s s m e n t

• Functional ability must be the focus when providing care to elderly people; this includes
evaluating ADLs, gait, cognition, and depression.
• Physical examination and identification of disease(s) do not sufficiently define the functional
ability of the patient.
• Using structured assessment tools identifies problems and monitors the patient over time.

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Falls
I. Assessment tools

A. Timed “Up and Go” Test

1. This is a reliable, valid, and practical test of balance and gait speed
2. To perform, time the patient as he or she rises from a standard
armchair, walks 10 feet, turns 180 degrees, returns to the chair, and sits
down again 3. The score is the number of seconds taken to complete
the test; a freely mobile person can complete it in <10 seconds. Further
evaluation is required if the test is not completed in 20 seconds.
4. The score(s) can be monitored to note clinical changes over time
B. Tinetti Balance and Gait Evaluation (see Table 3-12)
1. Assesses musculoskeletal and neurological disorders that increase the
risk of falls 2. Requires no equipment other than a hard, armless chair
3. Administered in 5 to 15 minutes in the clinical setting by observing
actual function 4. Activity-based test that asks the patient to perform
tasks such as sitting and rising from a chair, turning, and bending.
Scoring:
< 19 = high fall risk
< 19 to 24 = medium fall risk
< 25 to 28 = low fall risk
Table 3-12
Tinetti Balance and Gait Evaluation

Balance Tests
Instructions: Seat the subject in a hard armless chair. Test the following maneuvers and select
the number that best describes the subject’s performance in each test; add up the scores at the
end.
1. Sitting balance Leans or slides in the chair 0
Steady, safe 1
2. Arises Unable without help 0
Able, uses arms to help 1
Able without using arms 2
3. Attempts to arise Unable without help 0
Able, requires >1 attempt 1
Able to rise, 1 attempt 2

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 4. Immediate standing balance (first 5 s) Unsteady (swaggers, moves feet, 0
trunk sway) 1
Steady but uses walker or other 2
support
Steady without walker or other
support
Unsteady 0
5. Standing balance
Steady but wide stance (medial 1
heels >4 in apart) or uses cane, 2
walker, or other support
Narrow stance without support
Begins to fall 0
6. Nudging (with the subject’s feet as close together
Staggers, grabs, catches self 1
as possible, push lightly on the sternum with the
palm of the hand 3 times) Steady 2

7. Eyes closed (same position as in the previous Unsteady 0

exercise) Steady 1

8. Turning 360 degrees Discontinuous steps 0

Continuous steps 1
Unsteady (grabs and staggers) 0
9. Sitting down Unsafe (misjudged distance, falls 0
onto chair) 1
Uses arms or not a smooth motion 2
Safe, smooth motion
Balance score /16
Gait Tests
Instructions: Subject stands with the examiner, walks down the hallway or across the room,
first at the “usual” pace, then back at a “rapid, but safe” pace (using usual walking aids).
10. Initiation of gait (immediately after told to ‘go’) Any hesitancy or multiple attempts 0
to start No hesitancy 1
11. Step length and height: Does not pass left stance foot with a 0
step 1
Right swing foot: Passes left stance foot 0
Left swing foot: Right foot does not clear the floor 1
completely with a step 0
Right foot completely clears the 1
floor 0
Does not pass right stance foot with 1
a step
Passes right stance foot
Left foot does not clear the floor
completely with a step
Left foot completely clears the floor
12. Step symmetry Right and left step length not equal 0
(estimate) 1
Right and left step length appear
equal

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 13. Step continuity Stopping or discontinuity between 0
steps 1
Steps appear continuous
Marked deviation 0
14. Path (observe excursion of the left or right foot
over about 10 ft of the course) Mild/moderate deviation or uses 1
walking aid 2
Straight without walking aid
Marked sway or uses walking aid 0
15. Trunk
No sway but flexion of knees or 1
back or spreads arms out while 2
walking
No sway, no flexion, no use of arms,
and no use of walking aid
Heels apart 0
16. Walking stance
Heels almost touching while 1
walking
Gait score 12
Balance score (from previous page) 16
Total (gait + balance) /28
From Tinetti, M.E (1986). Performance-oriented assessment of mobility problems in elderly patients. Journal of the American Geriatrics
Society, 34(2), 119-126.

P r a c t i c e Pe a r l s f o r F a l l s

• Must include evaluation of balance and gait problems; gait disturbances in elderly people
are a risk factor for future cardiovascular diseases and dementia.
• Performed as part of an annual examination, as well as when there appears to be a change in
the patient’s health status.
• May be critical to include a home visit to assess both the patient and the environment for
prevention and safety.
• Elderly people often do not understand negative commands well; for example, say, “please
stay in bed (chair)” rather than “please don’t get out of bed (chair).”
• Risk factors for falls in elderly people

• Cardiovascular
■ Arrhythmias
■ Blood pressure fluctuation
■ CVA
• Musculoskeletal

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 ■ Arthritis
■ Joint weakness
■ Preexisting orthopedic conditions
■ Poor conditioning or inactivity
• Neurological
■ Dementia
■ Parkinson’s disease
■ MS
■ Vision and/or hearing loss
• Urinary or bladder problems
• Environmental
■ Wet or slippery surfaces
■ Cluttered paths (e.g., throw rugs, poor furniture arrangement) ■ Poor
lighting
■ Inadequate footwear (e.g., wearing socks without shoes) ■ Inadequate
supervision

*Only
additions to a normal health history are listed here.

105
CHAPTER 4

106
Laboratory and diagnostic pearls
General

I. Patient education: prelab instructions

A. Encourage drinking at least 8 ounces of water before the tests; may

drink all the noncaloric liquids desired (easier to obtain blood)
B. Do not eat anything for 8 hours before labs are drawn (while not all
tests require fasting, it is easier for the patient to remember if all are
performed in the same way)
C. May take medications at regular times
II. A normal test does not mean a healthy patient
III. With abnormal lab results, consider fluid status or medications (prescription, OTC, herbal)
first
IV. With dehydration

A. CBC: all cell lines (RBC, WBC, platelets) increase

B. UA: specific gravity increases and ketones often present
C. Chemistries: sodium increased, BUN/creatinine ratio >10

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Hematology (CBC)
I. General recommendations

A. All cell lines (RBC, WBC, and platelets) increase with

hemoconcentration (e.g., dehydration)
B. If two of three cell lines are abnormal (elevated or decreased), repeat
CBC in 24 to 48 hours; if still abnormal without a known cause (e.g.,
dehydration with infection), consider referral to a hematologist
C. With abnormal RBC, WBC, or platelet counts, recheck CBC along with
peripheral smear (gives a direct cell count and identifies any atypical
cells)
II. White blood cells

A. The normal neutrophil (seg) to lymphocyte (lymph) ratio is 60:40; the

percentage of segs may be elevated with infection, even with a normal
total WBC count; reverse ratio indicates lymphocytosis
B. “Shift to the left” (i.e., >5 bands [immature WBCs]) can occur with
increased, normal, or decreased WBC counts and indicates infection
C. Leukocytosis: WBC count generally >11,000 mm3; the reference range is
age-specific
1. “Greatly” elevated WBC count (e.g., >30,000 mm3) with
lymphadenopathy: suspect leukemia or lymphoma
2. Stress can increase WBC count to 20,000 to 25,000 mm3, with resolution
within ∼24 hours; this is more common in children
3. In patients aged >50 years, asymptomatic lymphocytosis often
indicates chronic lymphocytic leukemia. Refer to a hematologist.
4. Lymphocytosis plus anemia, thrombocytopenia, or neutropenia
suggests cancer; refer to a hematologist
D. Leukopenia: WBC generally <4000 mm3 in adults; age-specific ranges
in children
1. Decreased WBC with increased lymphocytes: viral infection, pertussis
2. In an immunosuppressed patient with neutropenia and any fever
>100.4°F without a clear cause: treat as a medical emergency (consider

108
 sepsis until proven otherwise)
E. Eosinophilia: consider allergies or helminth parasitic infection
III. Red blood cells, hemoglobin, hematocrit

A. Also see Anemia in Chapter 9 for more information on H&H and

reticulocytes
B. Normally, Hgb × 3 = Hct; if not, consider lab error
C. With chronic renal failure, baseline H&H is ∼10/30; if normal or
lower, there is an additional problem (e.g., “normal” with
dehydration)
D. Abnormal looking RBCs
1. Size denoted by MCV: normocytic means normal size
a) macrocytic: larger than normal
b) microcytic: smaller than normal
2. Amount of Hgb in RBCs is denoted by MCH: normochromic means
“normal color”; hypochromic means “pale” cells owing to less Hgb per
RBC
3. Anisocytosis means variation in the size of RBCs; denoted by elevated
RBC distribution width (RDW) count. This can be associated with
anemia.
4. Shape
a) schistocytes, helmet-shaped cells: fragmented RBCs due to destruction
within vessels (e.g., with TTP, DIC) or defective prosthetic valve
b) “tear-drops”: thalassemia, iron deficiency, other anemias
c) spherocyte: autoimmune hemolytic anemia, hereditary spherocytosis
d) “burr cells”: after splenectomy, uremia, malabsorption states
e) basophilic stippling: heavy metal poisoning (e.g., lead, arsenic),
thalassemia, hemoglobinopathies
E. If RBCs look abnormal or H&H counts are abnormal, repeat CBC
along with peripheral smear. If still abnormal, consider hematology
referral.
IV. Platelets

109
A. Normal platelet appearance does not mean that they function
normally
B. With abnormal platelet count, repeat CBC with peripheral smear; if
still abnormal, refer to a hematologist
1. Thrombocytosis (>450,000/µL): recheck in ≤1 week
a) types
(1) reactive: commonly caused by infection, after surgery, cancer
(2) chronic myeloproliferative: essential thrombocytopenia, polycythemia
vera, CML
(3) mild increase in platelet count: consider dehydration, chronic hypoxia
(COPD, chronic carbon monoxide poisoning in a patient who smokes)
b) associated with vasomotor symptoms (e.g., H/A, chest pain,
pain/burning in toes, lightheadedness) and thrombotic or bleeding
complications (less likely with reactive thrombocytosis)
2. Thrombocytopenia (<150,000/µL)
a) recheck platelet count
(1) with 100,000 to 150,000/µL: in 1 to 2 months
(2) with 75,000 to 100,000/µL in an asymptomatic, nonbleeding patient: in
1 to 2 weeks
b) bleeding risk
(1) 50,000 to 80,000/µL: may have petechiae (or be asymptomatic)
(2) 20,000 to 50,000/µL: bleeding risk increased
(3) <20,000/µL: highest risk for bleeding (may have spontaneous bleeding
at counts of <10,000/µL)
c) possible causes
(1) NSAID use does not usually cause a platelet count of <50,000/µL
(2) Idiopathic thrombocytopenic purpura (or immune thrombocytopenia;
ITP)
(3) drug related: condition usually resolves within 1 week after drug
cessation; ask about quinine-containing herbal products (e.g.,
cinchona, quina, Peruvian bark)

110
(4) viral: HIV, hepatitis C, CMV
(5) less common: liver disease with hypersplenism, myelodysplastic
syndrome

111
Urine
I. Urine specific gravity and serum sodium are the only tests that reliably vary with
hemodilution and hemoconcentration (see Table 4-1 for urinalysis findings)
II. Positive ketones: very nonspecific; consider dehydration first but also low-carb diet. Diabetic
ketoacidosis (DKA) is diagnosed with serum ketones.
III. Urine culture

A. Clean-catch urine culture recommended with suspected UTI: confirms

infection and guides antibiotic use
B. Positive results (from clean-catch specimen)
1. Asymptomatic patient: >100,000 CFU/ml
2. Symptomatic patient: 100 to 100,000 CFU/ml
IV. Proteinuria

A. From urinalysis or urine dipstick: see Table 4-1

B. From a 24-hour urine specimen
1. Minimal (<0.5 g/day): exercise or concentrated urine in a healthy
person; fever, cystitis, polycystic kidneys
2. Moderate (0.5 to 3 g/day): mild DM nephropathy, chronic
glomerulonephritis
3. Marked (>3 g/day): lupus nephritis, AGN, severe DM nephropathy,
amyloid disease
V. Albumin/creatinine ratio (ACR): CKD diagnosis if >17 mg/g (males) or >25 mg/g (females)
Table 4-1
Urinalysis Findings

Normal Findings Abnormal Findings Significance

Appearance: Colorless/pale Diabetes insipidus, alcohol, increased fluid intake, water
Clear, straw-yellow intoxication related to psychiatric meds
color

Red or brown Blood, porphyrin

Foods: beets, rhubarb, food color
Meds: sulfisoxazole, phenytoin, cascara, chlorpromazine,
rifampin, senna

Orange Decreased oral intake, urobilinogen, fever

Meds: phenazopyridine (Pyridium), sulfa, nitrofurantoin

112
 Foods: carrots, rhubarb

Blue or green Pseudomonas

Meds: amitriptyline, methylene blue
Vitamin B complex

Brown or black Hemorrhage, melanin, bilirubin, methemoglobin, myoglobin

Foods: cascara, senna, iron

Cloudy Bacteria, pus, prostatic fluid, semen

Milky Pyuria, hyperlipidemia

Foamy Cirrhosis, bilirubin, bile, hepatitis, obstructive liver disease,

proteinuria

Odor: Ammonia Urea breakdown, increased nitrites

Aromatic
Foul Bacteria

Mousy Phenylketonuria

Fruity DM, starvation or extreme dieting, anorexia, bulimia

pH: <4.6 Acidosis, high-protein diet, severe diarrhea/vomiting, severe

4.6-6.5 COPD, renal stones
Meds: metformin

6.5-8 Bacteriuria, UTI, metabolic alkalosis

Meds: neomycin, sulfa, potassium citrate

Specific gravity (reflects <1.005 Diabetes insipidus, increased oral intake

renal concentrating Meds: diuretics
ability):
1.005-1.030 >1.030 Decreased oral intake, dehydration, fever, excess
vomiting/diarrhea, iodine dye, DM

Protein: Positive Trace/1+: consider exercise and recheck early morning specimen
Negative If >2+, get 24-hr urine for Pyelonephritis, glomerulonephritis (1+ to 2+), bladder cancer, UTI,
protein and creatinine HF, myeloma, fever, lead poisoning, toxemia, DM, nephrosis (3+
clearance to 4+)
Meds: barbiturates, sulfa, neomycin

Glucose: Positive DM, CVA, anesthesia, extreme stress

Negative Meds: ASA, cephalosporin, vitamin C, epinephrine

Ketone: Positive High-protein diet, decreased oral intake, heat exhaustion, early
Negative DKA, fever, hyperthyroidism

Bilirubin: Positive Hepatitis, cirrhosis, obstructive gallbladder disease

Negative

Urobilinogen: >2 mg/dl Can be due to normal bile metabolism, HF, hyperthyroidism (also
<2 mg/dl see Figure 4-1)
Med: neomycin

Leukocyte esterase: Positive Infection

113
Negative

Nitrite: Positive Infection

Negative

Blood: Positive Kidney stones, cancer, infection, menses, transfusion reaction,

Negative trauma, Foley catheterization, polycystic kidneys
Meds: anticoagulants

Microscopic Findings
RBCs: >2/HPF Renal disease, kidney stones, cancer, UTI, strenuous exercise,
<2/HPF >3/HPF: repeat UA; if 2 trauma to GU tract
tests abnormal, evaluate Meds: ASA, warfarin sodium
further

WBCs: >4/HPF UTI, interstitial cystitis, AGN, fever, SLE, strenuous exercise, TB,
<4/HPF analgesic abuse

Epithelial cells: >5/HPF Usually indicates contaminated specimen

<5/HPF

Hyaline casts: 10-30/HPF Strenuous exercise, HF, fever, HTN, AGN

<5/HPF

RBC cast: >2/HPF AGN, renal cancer, SBE, vasculitis, GABHS, malignant HTN
none

WBC cast: >2/HPF Kidney inflammation (possible pyelonephritis, acute tubular

none necrosis)

Bacteria: >5/HPF UTI

none

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Liver
I. Liver function tests evaluate hepatocellular function

A. PT/INR (INR is a standardized way to report PT): prolonged with

liver disease, causing inadequate production of certain clotting factors
B. Albumin: controls osmotic pressure, which maintains fluid in blood
vessels
1. Decreased: leads to edema (e.g., in cirrhosis, liver failure, and
malnutrition; also in nonhepatic acute and chronic illnesses)
2. Increased: may indicate dehydration
II. Hepatocellular enzymes measure the severity of hepatocellular inflammation

A. ALT: more specific to the liver and less to the heart, muscle, and
kidney
B. AST: present in tissues with high metabolic activity and increased
with liver disease, tumor, MI, heat stroke
1. With elevated levels, first consider Alcohol-Statins-Tylenol (common
causes)
2. AST > 1000 IU/L is often due to infection or toxins (e.g., medications,
herbs, poisons); if occurs within the first 24 hours of illness, there is a
high likelihood that the patient will not survive
C. If AST/ALT levels are elevated but are <3× the normal: stop alcohol
and all OTC medications and supplements; recheck in 2 weeks before
performing any further tests. If still elevated after 6 months, refer to a
gastroenterologist.
D. AST/ALT ratio
1. Normally ∼1
2. Helps differentiate ETOH-induced liver damage from infectious
hepatitis
a) ALT > AST = infectious hepatitis
b) AST > ALT = alcohol-related damage (usually 3:1 to 8:1)
3. If >1: consider medications, viruses, autoimmune hepatitis,

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 hemochromatosis, Wilson’s disease, α-1-antitrypsin deficiency,
nonalcoholic fatty liver disease (NAFLD), a fast food–heavy diet
E. Biliary enzymes (e.g., alkaline phosphatase, bilirubin, and GGT) are
increased in cholestatic conditions (obstruction either within the liver
itself or affecting the bile duct [e.g., gallstone, pancreatic mass])
1. If alkaline phosphatase is the only elevated liver test, it often indicates
an infiltrative process (e.g., tumor mass). To confirm that it is from the
liver, obtain a GGT level (GGT is usually elevated in liver disorders
but not in bone disorders).
2. If GGT is the only elevated liver test, it may indicate excessive alcohol
use
3. Total bilirubin: function of Hgb breakdown; reflects the liver’s ability
to dispose of Hgb; increases with obstructive jaundice, stones, or
damaged liver cells
4. Bilirubin >3.5 mg/dl results in jaundice, which indicates an obstruction
in the bile duct area. Because no bilirubin should be excreted renally
(normally goes out in the bowel), check urinalysis for bilirubinuria
(Figure 4-1).

FIGURE 4-1 Bilirubin in Urine.

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III. Miscellaneous

A. Medications commonly associated with drug-induced liver injury

include acetaminophen, anabolic steroids, NSAIDs (especially
diclofenac), amiodarone, valproic acid, isoniazid, and azathioprine
B. Any medication can increase enzymes in susceptible people; people
with liver disease or cirrhosis are at no higher risk than the general
population
C. Always check TSH level; hypothyroidism may cause a mild increase
in liver enzymes
D. With abnormal enzymes, also check for hepatitis A, B, and C (see
Hepatitis Illness in Chapter 10)
IV. Refer to a gastroenterologist/hepatologist

A. With unexplained, persistent elevations of ALT and AST >2 × the

upper limit of normal (ULN) or alkaline phosphatase >1.5× ULN
B. Patients being considered for liver biopsy

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Chemistries
I. A change in serum sodium levels changes serum osmolality; if it occurs quickly, the patient can
experience neurological symptoms, so correct hyponatremia/hypernatremia over the time period
you think it has occurred
II. With hyponatremia, check serum and urine osmolality and urine electrolytes

A. Increased urine osmolality: dehydration, high-protein diet,

hypernatremia, hyperglycemia, SIADH
B. Decreased urine osmolality: DI, excess fluid intake, renal insufficiency,
glomerulonephritis
C. Serum osmolality >300 mOsm/kg: hyperglycemia (DKA or
hyperosmolar hyperglycemic state [HHS])
D. Serum osmolality <280 mOsm/kg: thiazides, severe liver or heart
disease
III. With low bicarb (metabolic acidosis), consider SLUMPED

Salicylates
Lactate
Uremia, Underfed
Methanol
Paraldehyde
Ethanol, Ethylene glycol
Diabetes
IV. There is an obligate renal loss of 40 mEq K+ daily; if the patient is NPO, consider adding KCl
to IV fluids
V. Blood urea nitrogen (BUN): the liver produces ammonia from protein breakdown, which
results in nitrogen; this is then transformed into urea, which is excreted by the kidneys. Thus
BUN can reflect liver or kidney dysfunction.

A. BUN increases with renal failure; creatinine will also be high

B. BUN increases with dehydration, GI bleeding, and high-protein diet
but creatinine is normal
C. With GI bleeding, BUN decreases within 24 hours of bleeding
cessation; thus, monitor BUN daily and if it increases, consider
recurrent bleeding even if not clinically apparent

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 D. BUN decreases with starvation (inadequate protein intake), liver
failure (inadequate production of urea), and overhydration
E. Normal BUN/creatinine ratio = 10; if >10, consider prerenal azotemia;
if <10, consider renal failure
VI. Cardiac enzymes may be helpful if positive, but if within normal limits, they do not rule out
MI (serial tests are needed)
VII. Amylase and lipase

A. Perforated ulcer is accompanied by increased amylase but not lipase

B. Although pancreatitis is a common cause of elevations, there are many
other causes. However, lipase elevated >3× the normal has 98%
sensitivity for pancreatitis.

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Miscellaneous
I. Vitamin D

A. Suspected deficiency: order 25-hydroxyvitamin D levels (not 1,25-

dihydroxyvitamin D); note: diagnoses that are covered with this lab
parameter include myalgia and myositis, osteoporosis, psoriasis,
hypercalcemia, bariatric surgery, and long-term use of medications.
Fatigue and malaise are not covered, nor is screening.
B. Vitamin D at 1000 IU daily will increase serum vitamin D levels by 7
to 10 ng/ml.
II. A1c (elevated)—also see Diabetes Monitoring, Section II in Chapter 16

A. Marker for accelerated ASCVD: every 1% increase in A1c increases the

risk of CV events by 20% overall and CV mortality by 24% (males) and
28% (females)
B. Increases the risk of HF after MI
III. Pulse oximetry (ox): noninvasive measurement of arterial O2 saturation

A. There is no defined abnormal level because there is no defined

threshold of tissue hypoxia. It is most helpful to know the patient’s
usual level, but “reasonable” abnormal values could be as follows:
1. Resting pulse ox ≤95%
2. Exercise desaturation ≥5% (should increase with exercise)
B. Possible causes of low values
1. COPD is the most common cause of hypoxia
a) only 10% to 20% of patients with COPD retain CO2
b) baseline O2 sat in COPD is 88% to 90%
2. Hypoventilation
a) CNS depression (e.g., drug OD, ischemic lesion impacting respiratory
center)
b) obesity
c) neurological (e.g., ALS, Guillain-Barre)
d) musculoskeletal (e.g., myasthenia gravis, muscular dystrophy,

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 kyphoscoliosis)
e) severe hypothyroidism

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Lab tests for arthralgias
I. Antinuclear antibody (ANA)

A. Negative test (<1:80) excludes systemic lupus erythematosus (SLE) in

95% of the cases
B. Positive titer (≥1:160) is more likely a true result, but can still be false
positive with chemo, cancer, some medications (e.g., INH,
procainamide, hydralazine)
C. Positive titer alone is not diagnostic of SLE. Refer to a rheumatologist
because the positive titer must be verified with other tests; tell the
patient, “The test shows inflammation in the blood, but other tests
need to be performed.”
II. RA factor

A. 80% sensitive in rheumatoid arthritis

B. False-positive results can occur in chronic infections and other chronic
inflammatory conditions
III. Erythrocyte sedimentation rate (ESR or sed rate)

A. Increased with anemia, inflammation, infection, obesity, cancer; may

exhibit mild to moderate increase with significant psychosocial stress
B. Elevated ESR with negative RA and ANA: suspect cancer
C. If >100 mm/hr: consider infection (33%), cancer, inflammation (e.g.,
temporal arteritis, polymyalgia rheumatica [PMR]), nephrotic
syndrome (a common cause is diabetic nephropathy)
D. If symptoms improve but ESR remains high, consider additional
causes of inflammation (e.g., temporal arteritis) or more aggressive
treatment
E. ESR changes more slowly than CRP as the patient’s condition worsens
or improves.
IV. C-reactive protein (CRP)

A. It is not known what level is truly normal or clinically innocuous;

serial tests are best
1. Used to guide management of RA

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 2. Elevated levels are definitely linked to ACS but not to stable angina
3. Increases with high-fat meal or foods sweetened with high-fructose
corn syrup
B. High-sensitivity CRP (hs-CRP) only means that the results were
determined using an assay to measure very low levels of CRP (i.e., <0.3
mg/L).
C. hs-CRP > 10 mg/L: often rheumatic cause, infection or inflammation;
recheck in 2 weeks
V. Uric acid

A. Not the only criteria used to diagnose gout; it can be used to monitor
the response to medications such as allopurinol
B. Before starting medication for elevated uric acid, consider the need for
a crystal-driven diagnosis of gout (i.e., joint aspiration)

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Radiology pointers
I. CXR: changes indicating pneumonia may lag 3 days behind clinical diagnosis (i.e., CXR may
appear normal but the patient has signs/symptoms of pneumonia). This is also why follow-up
CXR is performed 1 to 4 weeks after finishing therapy.
II. Carotid Doppler: 80% to 99% stenosis with/without symptoms indicates severe stenosis;
surgeon consultation recommended
III. Pelvic and transvaginal U/S recommendation

A. Order pelvic with suspected pelvic mass

B. Order transvaginal with suspected ectopic pregnancy, early pregnancy
of <9 weeks, or abnormal uterine bleeding (to check uterus and
endometrial lining)
IV. Contrast medium

A. Gastrografin: an oral contrast that does no harm if it enters the

peritoneal cavity (e.g., with bowel or stomach perforation)
B. Barium: an oral contrast that is contraindicated with suspected acute
abdomen
V. CT/MRI scans (also see Table 4-2)

A. With renal insufficiency, CT of the abdomen and/or pelvis with and

without ORAL contrast only
B. MRI scans of the spine are performed without contrast unless the
patient has a history of cancer, has had surgery in the area of the spine
within 2 years, or has infection
C. MRI scans of an extremity or joint are usually performed without
contrast; contrast is indicated to rule out soft tissue mass or
osteomyelitis
D. For pediatric patients: consider U/S before ordering CT or MRI
Table 4-2
CT and MRI Scans

Condition
Test Ordered (With or Without Contrast*) Notes
Considered
Head/brain
Acute bleeding CT brain w/o
Chronic bleeding MRI brain w/o MRI brain never with
contrast only

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 Aneurysm MRI brain w/ and w/o MRI brain never with
OR contrast only
MRA head w/o MRA head never
done with contrast
Head trauma CT brain w/o Contrast only if
indicated after first
scan
Pituitary/sella MRI w/ and w/o MRI brain never with
pathology contrast only
Mass/tumor CT brain w/ and w/o MRI brain never with
suspected OR contrast only
MRI brain w/ and w/o
Sinus Limited CT sinus Usually done w/o
Neck
Mass or lump in CT soft tissue of neck w/
neck
Salivary stone CT neck w/ and w/o
suspected
Chest
PE suspected CTA chest w/ and w/o
Any other CT chest w/
pathology
Abdomen/pelvis†
Kidney stones CT abdomen/pelvis w/ and w/o oral contrast Facility may have a
Hematuria “kidney stone
protocol”
Appendix CT abdomen/pelvis w/ and w/o oral and IV contrast U/S recommended
first in pediatric
patients
Kidney/adrenal CT abdomen w/ and w/o oral and IV contrast
glands
Diverticulitis/acute CT abdomen/pelvis w/oral and IV contrast
abdomen
Gallbladder CT abdomen w/ and w/o oral and IV contrast U/S recommended
first
Pancreatic tumor CT abdomen/pelvis w/ and w/o oral and IV contrast
Pelvic fracture CT pelvis w/o
Bladder pathology CT pelvis w/ and w/o oral and IV contrast
Spine
Any area with CT w/o
acute trauma
Any area w/o MRI w/o, unless infection suspected, <2 yrs after
acute trauma surgery of spine, or Hx of any cancer; then MRI w/
and w/o
Possible spinal MRI w/ and w/o
lesion
*
IV contrast, unless noted otherwise.

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†Abdominal
and/or pelvic CT: oral contrast if the suspected problem is in the gut, IV contrast if the suspected problem is vascular.

126
UNIT II

127
Common Conditions

128
OUTLINE

5. Skin conditions
6. Respiratory conditions
7. Eye, ear, nose, and throat conditions
8. Cardiovascular conditions
9. Peripheral vascular and hematologic conditions
10. Abdominal conditions
11. Gynecologic conditions
12. Common urinary tract conditions
13. Neurologic conditions
14. Musculoskeletal conditions
15. Pain
16. Endocrine conditions
17. Pediatric conditions
18. Psychiatric conditions

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CHAPTER 5

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Skin conditions
Disorders causing inflammation

Atopic dermatitis (eczema)

I. Description

A. Cases usually stem from familial predisposition to eczema

B. Lesions can be diffuse erythematous macules, papules, or scaly
plaques that may have grouped vesicles
1. Lesions associated with itch-scratch cycle and paroxysmal itching
2. May produce exudation with wet crusts and fissures; this increases the
risk of secondary bacterial infections and molluscum
C. Patients usually have abnormally dry skin that itches more at night
D. Distribution of lesions is common on the face, antecubital and
popliteal spaces, joints and other areas of friction; distribution of
lesions may be symmetrical, but may be isolated and/or discrete (see
color plate 5) E. Patients may have acute exacerbations with periods of
remission
F. Increased prevalence of flare-ups with food allergies; smoke exposure;
change in climate, perfumes, and cosmetics
II. Treatment

A. Primary goal: prevention and maintenance of symptoms to minimize

use of steroids
1. Increase ambient moisture with a humidifier
2. Increase oral hydration
3. Wear all-cotton clothing
4. Moisturizers should be used routinely 3 to 4 times daily
a) apply moisturizers on the skin immediately after bathing (Eucerin,
Aquaphor, mineral or baby oil) b) decrease the number of baths per
week; use only tepid water and mild soap (Dial, Dove, Aveeno, Basis)

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 c) ointments are better moisturizers in dry environments or for very
young children or infants d) apply moisturizers when not using
steroid ointments to prevent flare-ups
5. Apply sunscreen to all exposed areas whenever outdoors
6. Vitamin E: 400 to 800 IU daily > age 12 years
B. Prompt identification and treatment of flare-ups or infections will
improve overall outcomes
C. Drug therapy
1. First-line therapy is topical steroids (Table 5-1)
a) initial therapy with low-potency steroids (e.g., 0.5% to 1% OTC
steroids) bid on the face or skin folds; can use mid-potency steroids bid
on the trunk until symptoms resolve for moderate eczema b) use
steroids for the shortest amount of time
c) high-potency steroids would be reserved for the most severe flare-ups
and for the shortest amount of time
2. Second-line therapy for frequent, hard-to-control flare-ups with
moderate to severe symptoms is topical immunomodulators
(calcineurin inhibitors)
a) tacrolimus (Protopic) ointment 0.03% for children aged 2 to 15 years;
0.03% to 0.1% for children aged >15 years; apply to lesions bid b)
pimecrolimus (Elidel) 1% for people aged >2 years; apply bid to
lesions; can be used in sensitive areas where steroids may cause
serious or systemic reactions
3. Oral steroids in “burst” therapy can be used short-term for severe,
refractory cases; must be closely monitored for side effects 4. Oral
antihistamines for sedative effect as needed to break the itch-scratch
cycle; can cause drowsiness
a) diphenhydramine (Benadryl) 12.5 to 50 mg q6h or
b) hydroxyzine (Atarax) 10 to 100 mg q6-8h or
c) cetirizine 5 mg/ml and give 2.5 ml for 2 to 5 years of age; 5 to 10 mg for
>6 years of age qd or d) cyproheptadine (Periactin) 2 mg/5 ml syrup or
4 mg tab tid; dose dependent on age
5. Topical antihistamines have an increased potential to cause contact

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 dermatitis to already inflamed skin and can cause drowsiness
a) topical diphenhydramine cream or spray
b) doxepin (adults only) 5% cream daily as needed
6. Emollients can be used for maintenance therapy and are safe for any
age
a) nonprescription ceramide-based creams decrease water loss in skin
(e.g., EpiCeram, CeraVe) b) prescription ceramide-based creams are
safe for any age and decrease water loss (Atopiclair [emollient],
MimyX [emollient/keratolytic])
7. Suggested antibiotic therapy given for 7 to 10 days for secondary
infections:

Drug Pediatric Dose Adult Dose

Dicloxacillin<40 kg: 12.5-25 mg/kg/day ÷ q6h 125-250 mg q6h
>40 kg: 125-250 mg q6h
Cephalexin 25-50 mg/kg/day ÷ q6-12h 500 mg q12h
Erythromycin 30-50 mg/kg/day ÷ q6-8h 250-500 mg tid

III. Referral: if atopic dermatitis is severe or unresponsive to treatment, start therapy and refer to
a dermatologist

Table 5-1
Selected Topical Steroid Potencies

Potency Product Vehicle Sizes

Very high Betamethasone dipropionate Ointment 15 and 45 g
potency (Diprolene) 0.05%
Clobetasol propionate (Temovate) Cream, 15, 30, 45, and 60 g
0.05% ointment
Diflorasone diacetate (Psorcon) Ointment 15, 30, and 60 g
0.05%
High potency Desoximetasone (Topicort) 0.25% Cream, 15 and 60 g
ointment
Fluocinonide (Lidex) 0.05% Gel, ointment, 15, 30, 60, and 120 g
cream
Halcinonide (Halog) 0.1% Cream 15, 30, 60, and 240 g
Triamcinolone acetonide (Aristocort) Ointment 15 and 60 g
0.1%
Fluticasone propionate (Cutivate) Ointment 15, 30, and 60 g
0.005%
Diflorasone diacetate (Florone) 0.05% Cream 15, 30, and 60 g
Medium Triamcinolone acetonide (Kenalog) Cream 15, 60, and 80 g
potency 0.1%

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 Fluocinolone acetonide (Synalar) Ointment 15, 30, and 60 g
0.025%
Mometasone furoate (Elocon) 0.1% Cream 15 and 45 g
Flurandrenolide (Cordran) 0.05% Cream 15, 30, and 60 g
Hydrocortisone valerate (Westcort) Cream 15, 45, and 60 g
0.2%
Hydrocortisone butyrate (Locoid) Cream 15 and 45 g
0.1%
Low potency Alclometasone dipropionate Cream, 15, 45, and 60 g
(Aclovate) 0.05% ointment
Fluocinolone acetonide (Synalar) Cream, solution 15, 30, and 60 g; 20 and
0.01% 60 ml
Desonide (DesOwen) 0.05% Cream, lotion 15, 60, and 90 g; 60 and
120 ml
Prednicarbate (Dermatop) 0.1% Cream 15 and 60 g
Hydrocortisone (Hytone) 2.5% Cream, 15, 30, and 60 g
ointment
Hydrocortisone (OTC brands) 1% Cream, 15 and 45 g
ointment

Contact dermatitis

I. Description

A. Inflammation of the epidermis and dermis caused by irritative agents

or allergens
1. Latex dermatitis affects health care providers primarily, but can affect
the general population 2. Latex is found in home products and medical
supplies and facilities; there are some foods that cross-react with latex
IgE (Table 5-2)
B. Characteristics are itching, burning, redness, and swelling with well-
demarcated areas where the irritant/allergen has touched the skin;
scaly, vesicular, or maculopapular lesions appear in scattered, linear
(rhus lines), or clustered groupings in the area of direct contact (see
color plate 6) C. Uncontrolled scratching can cause secondary skin
infections and scarring
D. Scarring can be caused by actual direct contact and any secondary
infections
II. Treatment

A. Remove irritant and cleanse skin thoroughly with soap and water
B. Control itching with oral antihistamines (e.g., diphenhydramine,

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 hydroxyzine, cyproheptadine—see atopic dermatitis for dosing); may
cause drowsiness C. Topical treatment for relief of itching with
moderate-to-severe contact dermatitis
1. Aluminum acetate (Domeboro)
2. Oatmeal baths
3. Calamine lotion/spray
4. Vinegar in water 50:50 solution
D. Topical steroids, mid-potency applied 2 to 3 times qd (see Table 5-1)
1. With more severe reactions, oral prednisone may be needed in “burst”
therapy, especially if the reaction involves the face 2. Do not use
topical steroids in the diaper areas or on the face of infants/children
because of the risk of systemic or local reactions
Table 5-2
Common Products Containing Latex

At home Adhesives, balloons, baby bottle nipples, carpet backing, clothing, elastic,
condoms, diaphragm, gloves, pacifiers, rubber toys, shower curtains, window
insulation
In a Ambu bags, gloves, blood pressure cuffs, IV tubing, catheter tubing/tip, rubber
clinic/hospital pillows, medical office cervical dilators, rubber stoppers, dental dams, elastic
setting bandages, elastic support hose, stethoscope tubing, electrode pads, surgical
implants, endotracheal tubes, tourniquets
Foods that Common foods: avocado, banana, chestnut, cantaloupe, kiwi, potato, tomato
may cross- Reported foods: apple, mango, peach, spinach, celery, melon, pear, turnip,
react with cherry, papaya, pineapple, wheat
latex

Xerosis (xeroderma)
I. Description

A. Moderate-to-severe dry, scaly, rough skin that is mildly pruritic and

appears on the extremities and “high use” skin areas (outer thighs,
buttocks, mid-back, extremities, feet/hands); usually spares the face
and scalp B. Occurs predominantly in winter and with lower humidity
C. May have pruritus with no obvious rash
II. Treatment involves conservation of skin moisture from evaporation and exposure; prevention
and maintenance of symptoms is essential to decrease use of steroids

A. Increase ambient moisture with a humidifier

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 B. Limit bathing and use tepid water and mild soap to decrease moisture
loss
C. Lubricants/emollients 3 to 4 times qd and after bathing
1. Vaseline, mineral oil, baby oil
2. Eucerin, Lubriderm, Aquaphor
3. Liquid vegetable shortening can be used and is cost effective
4. Apply lubricant to feet or hands at bedtime and wear white cotton
socks and/or gloves to bed. Wear the same socks or gloves every night
if there are no excoriations (could lead to secondary infection) as this
can decrease the amount of lubricant needed. This will soften callused
areas, especially on feet.
D. Ammonium lactate topical (Lac-Hydrin): bid and rub in thoroughly
E. Lactic acid creams (Eucerin Plus, Lacticare 5%): apply 3 to 4 times qd;
can alternate ammonium lactate and lactic acid creams if the skin is
sensitive F. Can use low-to mid-potency topical steroids 1 to 2 times
daily (see Table 5-1)

Urticaria (hives)

I. Description

A. Transient eruptions of papular lesions anywhere on the body

1. Any size from mm to inches or greater
2. Can last for <1 hour up to weeks and is usually pruritic
B. Associated with ingestion of drugs, foods, fish, and berries (e.g.,
allergic reactions) and occasionally with infection, trauma, stress, and
temperature changes C. Evaluate for angioedema and respiratory
distress
D. Evaluate psychosocial stressors for cause of urticaria
E. If chronic urticaria (>6 weeks) is present, check CBC, ESR, ANA, and
TSH to rule out systemic diseases
II. Treatment

A. Avoid triggers
B. Pharmacologic treatment

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 1. Urgent treatment for angioedema or respiratory distress
a) epinephrine 0.1 to 0.3 ml SQ may repeat in 15 to 30 minutes
b) diphenhydramine 25 to 50 mg PO or IV
c) O2 therapy
d) transport to ED
2. OTC medications for less severe urticaria (i.e., no angioedema or
respiratory distress)
a) H1 blockers: hydroxyzine 10 mg or diphenhydramine 12.5 to 50 mg q4-
6h or nonsedating antihistamines (e.g., fexofenadine, cetirizine,
loratadine) qd for 2 weeks b) H2 blockers may decrease reaction on a
daily basis (e.g., ranitidine 150 mg 1 to 2 times qd)
3. Prescription treatment
a) may need to start oral steroids in short-course “burst” therapy or dose
pack
b) leukotriene receptor antagonists may be recommended for cold
urticaria (e.g., montelukast 10 mg qd for adults and 4 to 5 mg daily
based on age) c) cyproheptadine (H1 blocker) 2 mg/5 ml, 0.25
mg/kg/day divided q8-12h for children; 4 mg qid for adults d) doxepin
(H1 and H2 receptor antagonist) 10 mg orally bid-qid
4. Chronic urticaria may need daily oral antihistamines H1 and/or H2
blockers for maintenance therapy 5. If chronic urticarial itching is not
relieved at night with oral antihistamines, try switching to tricyclic
antidepressants such as doxepin 10 to 50 mg at bedtime (adults only)
III. Refer to a dermatologist if there is no improvement in symptoms

Diaper dermatitis

I. Description

A. Inflammation occurs in the diaper area of infants or elderly people

who wear incontinence diapers/pads (see color plate 7) B. Usual cause
is irritation from urine/stool in close contact with the skin for long
periods of time or highly acidic urine/stool
1. Causes skin breakdown and secondary bacterial infection

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 2. Candida is the most common agent (see color plate 8)
C. Lesions are bright red and beefy in the diaper area, with papular and
sometimes pustular lesions; satellite lesions are common; lesions may
spare inguinal folds D. More common with history of atopic
dermatitis/eczema
II. Treatment (for any patient using protective undergarments for incontinence)

A. Frequent diaper changes

B. Discourage use of diaper wipes; if infant, bathe in tepid bath after
stooling/urinating and use dabbing technique instead of wiping or use
a spray bottle to cleanse the area C. After performing skin care, leave
the diaper area open to air or use a blow dryer on low setting at arm’s
length from the baby/adult after each diaper change D. Encourage use
of a barrier cream/ointment with each diaper change (e.g., zinc oxide,
white petroleum, or Aquaphor) E. Encourage using super-absorbent
diapers if frequent diaper changes are not an option, and avoid rubber
pants F. Discourage use of highly acidic foods/juices when dermatitis
is present
G. Use topical antifungals if Candida infection is suspected (nystatin
cream, clotrimazole, miconazole); apply 2 to 3 times qd to the diaper
area; use protective cream over this; consider oral diflucan therapy for
adults for recurrent or refractory Candida H. With worsening
inflammation, a combination steroid and antifungal
(nystatin/triamcinolone topical [Mycolog II ointment]) preparation
applied 2 times qd for a short period of time to the diaper area until
improvement (e.g., 1 week) I. If the mother is breast-feeding, consider
the possibility of thrush in the infant and treat both simultaneously

Seborrheic dermatitis

I. Description

A. Inflammatory papulosquamous dermatitis that affects sebaceous areas

B. Characterized by mild-to-severe red, dry, flaky, patchy lesions on the
face, ears, scalp, and trunk (see color plate 4) C. Patches are poorly
defined and appear greasy over inflamed skin with mild itching or
burning sensation D. Lesions typically appear on nasolabial folds, ears,
eyebrows, or hairline; can occur in the groin, axilla, and mid-chest

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 areas E. Usually chronic condition with a bothersome appearance
II. Treatment

A. Low-or mid-potency steroids can be used sparingly to control flare-

ups; caution the patient not to use steroids on the face for >5 days (see
Table 5-1) B. Selenium sulfide shampoo, ketoconazole shampoo (i.e.,
can use on face) to cleanse areas daily; leave on for ∼10 minutes and
then rinse off C. Ciclopirox for 4 weeks: topical gel 0.77% bid or
shampoo 1% 2 times a week; either can be used for anyone >16 years
D. Can use zinc pyrithione and salicylic acid for outbreaks
E. Gentle cleansing with a soft toothbrush to remove patches/plaques
III. Refer if unresponsive to treatment

Hyperhydrosis

I. Description

A. Excessive sweating, which can be localized or generalized,

predominantly noted in the axilla, groin, or palms of hands and soles
of feet B. Can disrupt lifestyle and cause embarrassment in social
settings
C. Symptoms do not occur at night
D. Begins in childhood or adolescence; if adult onset, look for a
secondary cause; condition will decrease as the person ages E. Usually
has a positive family history
II. Treatment

A. Start treatment with an OTC antiperspirant (not deodorant) to block

sweat production (e.g., Certain Dri) and use at night B. Pharmacologic
treatment
1. Apply aluminum chloride 20% (Drysol) for 7 to 10 nights initially, then
1 to 2 times a week; wash off every morning 2. Aluminum chloride
6.25% (Xerac AC) at night to the axilla and palms
3. Oxybutynin 1.25 to 5 mg po bid
4. Can try Botox injections for axillary sweating (off-label use approved
by FDA)
C. Sweating and tachycardia associated with social phobia and/or public
speaking may be relieved with propranolol 10 to 20 mg

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III. Refer to a dermatologist if uncontrolled or if the condition is affecting life

Psoriasis

I. Description

A. Familial tendency; the condition usually starts in childhood

B. Lesions are inflamed, thickened, pruritic, violaceous plaques with
powdery white or silver scales (see color plates 9 and 10)
1. Lesions vary in size and distribution; most common over extensor
aspects of elbows and knees, presacral area, ears, and scalp, but can
occur anywhere 2. Pustules most common on palms and soles but can
have guttate psoriasis, which involves skin over most of the
torso/extremities
C. Pitting and dystrophy of nails
II. Treatment

A. Topical treatment
1. Emollients to maintain skin hydration and minimize itching
2. Mid-or high-potency steroids (see Table 5-1) for up to 5 days on the
skin for acute exacerbations; use low-potency steroids in intertriginous
areas 3. Small, mild, hyperkeratotic lesions respond to low-potency
topical steroids (hydrocortisone 1%) with tar preparations (e.g.,
phototar or anthralin) 1 to 2 times qd 4. Scalp lesions often require tar
shampoo, salicylic acid, and/or steroids under an occlusive shower cap
to increase contact time 5. Calcipotriene topical 0.005% (Dovonex)
applied bid; avoid face, mucous membranes, and eyes; wash hands
after application
a) can combine calcipotriene and a topical steroid cream to get greater
benefits with a decreased side effect profile b) combining calcipotriene
and UVB exposure can improve treatment (caution the patient that
calcipotriene should be administered after UVB treatment)
6. Tazarotene topical cream/gel 0.05%, 0.1% (Tazorac) applied qhs; if the
patient is of child-bearing age, perform pregnancy test before starting
treatment
a) effective in decreasing scales and can be used as monotherapy for
chronic plaques

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 b) most common side effect is local irritation; irritation is decreased when
tazarotene is combined with topical steroids c) combining tazarotene
with UVB light therapy can result in quicker remission, but the UVB
dose must be lowered because of an increased risk of burning
B. Discourage scratching and rubbing of lesions
C. Discourage oral steroids
D. Psoralen ultraviolet A-range (PUVA) treatment may relieve
symptoms; can also try tanning bed phototherapy
III. Refer to a dermatologist if unresponsive to treatment

P r a c t i c e Pe a r l s f o r T o p i c a l S t e r o i d s

• Topical steroids are antiinflammatory agents that control inflammation and pruritic
conditions of the skin. Remember to consider the potency, location, and desired duration of
action when prescribing a topical steroid preparation. (See Table 5-1 for selected topical
steroid potencies; this list is not all-inclusive.) • High-potency steroids

• Do not use “very-high-potency” steroids on the face or groin area or with

occlusive dressings.
• Topical steroids, especially at higher concentrations and in children,
can affect the HPA axis; beware of the dosage and slowly withdraw the
drug if it has been used for a long time.
• When a high-or very-high-potency steroid is ordered, indicate on the
prescription “not for use on the face.”
• Use of steroid pulse therapy (i.e., using moderate-to-high doses of
steroids daily for <5 days) will decrease the chance of tachyphylaxis;
there should be an interval of at least 1 month between pulse therapies.
• Pediatric use

• Do not use topical steroids for diaper rash; children have a greater
body surface area; therefore, absorption will be greater.
• For an infant <6 months of age, low-potency steroids (e.g., 1% OTC
hydrocortisone) can be used for <7 days.

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• For a child aged 6 months to 12 years, mid-potency steroids can be
used for short periods of time (e.g., 7 to 10 days).
• Use after bathing to enhance absorption.
• Twice-a-day application is most useful and economical; more frequent applications do not
hasten improvement because topical steroids have a repository effect; start with bid
applications and decrease as improvement occurs.
• Adverse reactions such as skin thinning, striae, rebound lesion flares, and HPA axis
suppression can occur.
• Vehicles for administration: steroids come in various vehicles to maximize effects

• Ointments are more occlusive; use for dry, cracked, scaly lesions; more
potent than creams or lotions in the same group; may cause maceration
and folliculitis; do not use on open, draining wounds.
• Creams are less occlusive and more drying; used for oozing lesions and
in intertriginous areas; increase anesthetic action; rub in well; these are
good for treating dermatitis in hot, humid climates.
• Gels, lotions, foams, and aerosols: gels have some occlusive properties;
gels and foams are used on hairy areas; urea-containing creams
increase skin hydration, facilitate cortisone penetration, and may be
cooling to the skin; lotions are better for use on the face.
• Occlusive dressings

• Can be used in areas where increased uptake of topical steroids is

required
• Should not be used for >12 hours qd because of enhanced penetration
and concomitant systemic effects • Patient instructions regarding
occlusive dressings:
■ Soak the area in warm water or wash well with warm water.
■ While the skin is still slightly wet, rub the topical steroid into the
affected area (increased moisture increases penetration).
■ Cover the area with a plastic wrap, such as Saran Wrap, and seal the
edges with tape or a cloth bandage; ensure a good seal between the
steroid and the skin; gloves may be worn on the hands; sandwich bags
for the feet and shower caps for the scalp may also be used.
■ Leave the dressing in place overnight or approximately 6 hours; do not
use an occlusive dressing with very-high-potency steroids.

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 ■ Patients should report signs of infection such as pain, increased
warmth, exudate, and worsening redness to the practitioner;
discontinue occlusive dressing immediately.
• Some conditions may require oral steroid therapy (Table 5-3).

Table 5-3
Oral Steroid Equivalency

10 15 20 25 30 40
Name 5 mg 35 mg
mg mg mg mg mg mg
Prednisone or prednisolone 5 mg tablets 1 tab 2 tab 3 tab 4 tab 5 tab 6 7 tab 8 tab
tab
Prednisone 5 mg/5 ml (liquid Pred syrup) 1 tsp 2 tsp 3 tsp 4 tsp 5 tsp 6 7 tsp 8 tsp
tsp
Prednisolone 15 mg/5 ml (Prelone syrup) 1⁄3 2⁄3 1 tsp 1.3 1.6 2 2.3 2.6
tsp tsp tsp tsp tsp tsp tsp
Dexamethasone 0.5 mg/5 ml (Decadron 1.5 3 tsp 4.5 6 tsp 7.5 9 10.5 12
elixir) tsp tsp tsp tsp tsp tsp
Prednisolone sodium phosphate 5 mg/5 ml 1 tsp 2 tsp 3 tsp 4 tsp 5 tsp 6 7 tsp 8 tsp
(Pediapred) tsp
Methylprednisolone 4 mg tablets (Medrol) 1 tab 2 tab 3 tab 4 tab 5 tab 6 7 tab 8 tab
tab
Triamcinolone 4 mg tablets (Aristocort) 1 tab 2 tab 3 tab 4 tab 5 tab 6 7 tab 8 tab
tab

Acne

I. A disorder involving chronic inflammation of the pilosebaceous follicles, probably involving

an increase in androgenic hormones; usually occurs in adolescents and has a familial tendency;
may disrupt lifestyle because of appearance of the skin II. Age-specific acne

A. Neonatal and infantile (up to 12 months of age) acne are more

common in males. Typically closed comedones are noted on forehead,
nose, and cheeks; usually caused by androgen excess; usually resolve
by 3 to 4 months of age. If severe, this could be linked to endocrine
disorders.
B. Mid-childhood acne (1 to 7 years of age) is not common because of
decreased circulating androgens; the patient should be referred to
pediatric endocrinologist C. Preadolescent (7 to 17 years of age)
1. Common sign of maturation
2. Usually comedomal with “T zone” distribution (forehead and central
face)

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 3. Few inflammatory lesions
4. No work-up unless concern for glandular abnormality such as PCOS
III. Grades of acne and treatment

A. Grade I (mild): few comedones or mixed appearance, no erythema,

and few papules (see color plate 1)
1. Wash skin once or twice daily using hands to avoid trauma, not a cloth
or buff puff; do not rub the skin 2. Avoid harsh soaps; use OTC acne
wash such as Neutrogena acne wash, Whitedove, or Cetaphil; pat skin
dry; do not rub skin 3. As monotherapy, start with benzoyl peroxide
(BP) 2.5% or higher with current regimen from above initially for 4
weeks (Table 5-4) 4. If no improvement, apply a retinoid (see Table 5-
4); start with a low dose and gradually increase as needed 5. Apply
moisturizer over the retinoid to prevent erythema and skin drying
6. If response is inadequate after 4 weeks of same treatment, change to
combination treatment by increasing the concentration or formulation
of topical retinoid or apply topical antibiotic (alone or in combination
with retinoid or benzoyl peroxide)
a) erythromycin: Akne-Mycin
b) erythromycin/BP: Benzamycin
c) clindamycin: Cleocin T
d) clindamycin/BP: Duac, BenzaClin
e) clindamycin/tretinoin: Ziana
f) sulfacetamide: Klaron
g) sulfacetamide/sulfur: Clenia
7. Apply a topical antibiotic cream, gel, or solution in the morning and a
retinoid at night; always use a moisturizer over the retinoid at night
and a moisturizer in combination with a sunscreen in daytime
B. Grade II (moderate) acne presents with moderate amount of
comedones with increasing papular and pustular lesions and mild-to-
moderate erythema
1. Treatment is the same as with Grade I acne, but add an oral antibiotic
bid until lesions start to resolve; the patient may need qd dosing until
the condition is resolved. Oral antibiotics may be needed

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 intermittently to control outbreaks (Table 5-5).
2. Maintenance antibiotics are same as those listed above except that
dosing is daily; a patient could take antibiotics for years 3. Continue
with benzoyl peroxide and retinoid even when on oral antibiotic
4. Consider dapsone (Aczone) with antibiotics
5. If androgen excess is the predominant cause of acne, the female patient
can try oral contraceptives (see Tips on Taking OC, Chapter 11) or
spironolactone 6. People of color will scar more easily and have
increased depigmentation and may require more aggressive treatment
with combinations of benzoyl peroxide, retinoids with antibiotics, or
oral antibiotics 7. Refer to dermatologist if response is poor
C. Grade III (severe): pustular, nodular, and cystic lesions, and erythema
1. Treatment aimed at avoiding scarring or disfigurement
2. Oral antibiotics plus topical retinoids plus benzoyl peroxide with or
without oral antibiotics 3. Add hormonal therapy for females
4. Dermatologist referral for consideration of isotretinoin (Accutane) and
other therapies if needed
IV. Variants of acne may be caused by the following:

A. Pressure, friction, or rubbing (e.g., acne beneath the hatband)

B. Some oil-based cosmetics; acne usually resolves when cosmetics are
not used
C. Overuse of topical steroids; when the steroid is stopped, acne will
resolve
Table 5-4
Topical Acne Medications

Benzoyl Peroxide Retinoids Moisturizers

Benzac AC and Benzac W Retin-A (tretinoin) Cetaphil
Benzoyl peroxide 4% or 5% Differin (adaptaline) Purpose
Brevoxyl Azelax (azelaic acid) Neutrogena
Triaz 3%, 6%, 9% Tazorac (tazarotene) Clinique
ZoDerm 4.5%, 6.5%, 8.5% Epiduo (adaptalene+benzoyl peroxide)
Desquam X Aveeno Clear complexion (salicylic acid)

Table 5-5
Oral Antibiotics for Acne

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 Drug Dosages Cautions
Tetracycline Adolescent*: 125-250 mg bid for 1 May cause sun sensitivity
wk, then qd Always use a sunscreen
Adult: 250-500 mg bid

Minocycline 50-100 mg qd-bid May cause sun sensitivity

IR >12 years:1 mg/kg/qd Always use a sunscreen
or May cause dizziness or vertigo
Minocycline
ER
Doxycycline 50-100 mg qd-bid May cause sun sensitivity
Always use a sunscreen
Erythromycin 250-500 mg qd-bid GI upset
Drug to drug interactions
Ampicillin 250-500 mg bid May cause diarrhea and increased risk of
yeast infection
TMP-SMZ DS 160/800: 1 tab bid May cause sun sensitivity
*Adolescent
is defined as a person aged 13 to 17 years.

P r a c t i c e Pe a r l s f o r A c n e

• Therapies for acne are time consuming and involve commitment of the person to a daily
regimen of care; resolution is very slow, and continual reinforcement is needed.
• Always obtain a detailed history of the patient’s symptoms, including all OTC and
prescription drugs used and the use of “friend’s” cures for acne.
• Sunscreens greater than 30 SPF and moisturizers are required daily.
• Topical products

• Tea tree oil may reduce the number of papules and comedones.
• Topical gels seem to work better in females; topical solutions (roll-ons)
are better tolerated by males; if the skin is dry, use creams; if the skin is
oily, use gels.
• Retinoids decrease follicular plugging but cause erythema of the skin;
encourage use of moisturizers over retinoids at night.
• Discourage picking at papules or squeezing bumps.
• Make-up brands that do not normally irritate acne are Almay, Neutrogena, Clinique, or any
that are accurately labeled as hypoallergenic.
• Suggest a low-glycemic diet and avoidance of junk foods. This does not worsen or have any
effect on acne per se, but most teenagers with significant acne are usually obese to some

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 extent and eat as a comfort measure.

Rosacea

I. Description

A. Rosacea is a cutaneous vascular disorder that develops later in life,

usually between 30 to 50 years of age, and is most common in fair-
skinned people; women are affected 3 times more often than men, but
men have more severe symptoms, including rhinophyma (see color
plate 2) B. Distribution of lesions occurs on the center of the face
(cheeks, chin, nose, or forehead), with inflammatory papules and
pustules on an erythematous base C. Many have flushing and blushing
reactions to emotional or environmental triggers (before actual lesions
occur)
1. Alcohol ingestion
2. Irritating cosmetics
3. Excessive washing of face
4. Emotional stress
5. Spicy foods, smoking, caffeine, or sun exposure
II. Signs and symptoms

A. Occurs bilaterally without comedones; there is very little to no

scarring
B. Central facial flushing (transient)
C. Nontransient erythema or persistent redness of the face
D. Papules and pustules in clusters
E. Telangiectasia
F. Burning or stinging, which can occur with the use of sunscreens or
moisturizers
G. Plaques and dryness with itchy, scaly skin (resembles xerosis)
H. Edema after prolonged flushing
I. Rhinophyma (usually in men)
J. Ocular manifestations

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 1. Watery, bloodshot eyes; dryness with photophobia
2. Conjunctivitis and blepharitis
III. Treatment

A. Topical pharmacologic treatment

1. Metronidazole 1% cream qd or metronidazole 0.75% gel bid
a) if severe, may need to add an oral antibiotic (tetracycline) until
remission
b) may take several weeks for the effects to be seen and the usual course
of treatment is up to 2 months
2. Clindamycin 1% lotion bid, erythromycin 2% solution bid, or
sulfacetamide/sulfur 10% qd to bid; treatment course may take up to 2
to 3 months 3. Azelaic acid (Azelac) 15% to 20% cream: apply bid up to
3 months (effective for papulopustular acne rosacea) 4. Ivermectin
cream 1% (Soolantra) apply qd
5. Antibiotics (either oral or topical) are not curative, may need to repeat
dosing later with flare-ups
B. Systemic therapy is used to treat hard-to-control rosacea with or
without ocular manifestations; treatment therapy may take up to 3 to 6
months
1. Tetracycline 250 to 500 mg q12h until improvement is seen; then
decrease to daily
2. Doxycycline 100 mg bid until improvement is seen; then may need
daily dosing
3. Minocycline 50 to 100 mg bid until improvement is seen; then may
need daily dosing
4. Metronidazole 250 mg qd for 4 to 6 weeks
C. Avoid using steroids on the face
D. Daily facial moisturizers, sunscreens, and mild cleansers
E. For flushing, consider clonidine 0.05 mg bid
IV. Refer to a dermatologist if symptoms are unresponsive

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Disorders caused by infection
Impetigo

I. Description

A. Highly contagious infection of the skin, usually seen in children

B. Caused by Staphylococcus aureus or group A β-hemolytic streptococci
1. Bullous impetigo (neonates or older infants) usually caused by S.
aureus
2. Nonbullous impetigo (most common type) seen in all ages of mobile
children, usually caused by group A β-hemolytic streptococci
C. Initial lesion is a vesicle that ruptures and becomes encrusted with
thick, honey-colored fluid, followed by the crust; usually found on
exposed skin (see color plate 11) D. Can be itchy and painful and is
quite contagious, but does not have associated constitutional
symptoms
II. Treatment

A. Improve overall hygiene and keep fingernails short

B. May need oral antihistamines (e.g., diphenhydramine) at night to
prevent scratching; can have the child wear gloves at night C. Gently
soak and remove the crust with an antibacterial soap
D. Topical treatment can be used if few lesions are present
1. Mupirocin tid for 7 to 14 days and cover with bandage
2. Retapamulin (Altabax) bid for 5 days and cover with bandage
E. Systemic oral antibiotic treatment for 5 to 10 days

Drug Pediatric Dose Adult Dose

Amoxicillin/clavulanate <3 mos: 30 mg/kg/day ÷ q12h 500/125-875 q8-12h
>3 mos, <40 kg: 25-45 mg/kg/day ÷ q12h
Cefuroxime 3 mos to 12 yrs: 30 mg/kg/day ÷ q12h 250-500 mg bid
Cephalexin 25-50 mg/kg/day ÷ q12h 500 mg q12h
Dicloxacillin <40 kg: 12.5-25 mg/kg/day ÷ q6h 125-250 mg q6h
>40 kg: 125-250 mg q6h

F. No daycare or school until 48 to 72 hours after antibiotics started

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 G. Culture the lesion if there is no response to treatment. This condition
usually resolves within 10 days of starting treatment
III. Refer if not responding to treatment

Scarlet fever rash

I. Description

A. Caused by group A β-hemolytic streptococci; considered to be a

serious infection because of the potential for migration of the bacteria
to the heart valves or kidneys B. Rash associated with “strep
pharyngitis”
1. Usually described as a red “sandpaper-like” texture with fine
maculopapular appearance that starts 1 to 2 days after the onset of
pharyngitis (although rash can be the first sign) 2. Starts around the
axilla, groin, and neck and then moves to the torso (the rash blanches
with pressure) (see color plate 14)
C. The tongue can be roughened and red with raised papules (strawberry
tongue)
D. For signs and treatment of strep pharyngitis, see Chapters 7 and 17
II. Referral

A. To ED if symptoms of tonsillar abscess occur or symptoms worsen or

respiratory distress occurs B. Consider referral to ENT if the person
has tonsils and has had three episodes in 1 year, causing difficulties for
the family because of leave from work or if the child is often missing
school

Erysipelas

I. Description

A. A superficial form of cellulitis with lymphatic involvement; has

sudden-onset redness with a well-demarcated, elevated border that is
advancing with swelling and pain
B. This is an aggressive infection that can lead to bullae, ulcers, and
necrosis
C. Most common sites are the face, hands, and lower legs, but can occur
anywhere

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 D. Often associated with constitutional symptoms such as fever, chills,
malaise, lymphadenitis
II. Treatment

A. Immobilize and elevate the extremity and use warm moist compresses
frequently
B. Infection is usually susceptible to antibiotics, with rapid improvement
within 24 hours C. Start oral antibiotic therapy for 10 to 14 days

Drug Pediatric Dose Adult Dose

Amoxicillin/clavulanate <3 mos: 30 mg/kg/day ÷ q12h 500/875 mg q8-12h
>3 mos, <40 kg: 25-45 mg/kg/day ÷ q12h
Dicloxacillin <40 kg: 12.5-25 mg/kg/day ÷ q6h 125-250 mg q6h
>40 kg: 125-250 mg q6h
Cephalexin >3 mos: 25-50 mg/kg/day ÷ q12h 500 mg q12h
Ciprofloxacin Not for children 500 mg bid

D. Recheck the patient in 24 hours and if the condition is worsening,

send to ED. Hospitalization should be considered for very young,
immunocompromised, or debilitated people if not improving rapidly.

Cellulitis

I. Description

A. Infected skin wounds, usually caused by Streptococcus or

Staphylococcus infections B. Erythema
1. Painful, warm erythema with poorly defined margins; usually follows
the lymphatic channel and gives the appearance of “streaking” on the
skin 2. Most frequently occurs in the head and neck in children and in
the lower extremities in adults, but can be found anywhere (see color
plate 13)
C. Constitutional symptoms may be present with fever, tachycardia, and
malaise
D. Suspect MRSA with abscess if the infection does not respond to
treatment, and obtain wound culture E. In elderly patients, infection in
the lower extremities may be complicated by edema and/or DVT
F. Consider hospitalization with poorly controlled DM, in an
immunocompromised person, or if the wound appears to be
necrotizing

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 1. Bullae formation or crepitus and any skin anesthesia
2. Discoloration affecting the limb or edema beyond the area of erythema
3. Ill-appearing person
II. Treatment

A. Reassess the patient in 24 hours

B. Warm moist compresses to the area 4 to 5 times qd
C. Keep the area elevated and at rest
D. Inquire about tetanus prophylaxis (see Table 5-6 for tetanus
prophylaxis) E. Oral antibiotic therapy for 7 to 10 days

Drug Pediatric Doses Adult Doses

Amoxicillin/clavulanate <3 mos: 30 mg/kg/day ÷ q12h 500/875 mg q8-12h
>3 mos, <40 kg: 25-45 mg/kg/day ÷ q12h
Dicloxacillin <40 kg: 12.5-25 mg/kg/day ÷ q6h 125-250 mg q6h
>40 kg: 125-250 mg q6h
Cephalexin 25-50 mg/kg/day ÷ q12h 500 mg q12h
Cefdinir 6 mos to 12 yrs: 14 mg/kg/day ÷ q12h 300 mg q12h
Ciprofloxacin Not for children 500 mg bid
TMP-SMZ 80/400: 8-10 mg/kg/day ÷ q12h 160/800: 1 tab bid
Clindamycin 30-40 mg/kg/day ÷ q6-8h 150-300: q6h

F. Refer severely ill patients to ED for hospitalization and IV antibiotics

Table 5-6
Postexposure Tetanus Prophylaxis for People Who Previously Received Tetanus Toxoid
Doses

Significant Wounds* Minor Wounds

Tetanus
Vaccine† Tetanus Immune Globulin Vaccine† Immune
Globulin
Unsure of the Yes Yes (do not mix vaccines and Yes No
tetanus status or do not give in the same
<3 doses extremity)
Has had at least 3 Yes, if the last No Yes, if the last No
doses dose was >5 dose was >10
yrs ago yrs ago
*Including contaminated wounds, those related to necrotizing infections, or those from crush injury, burns, frostbite, bullets, or shrapnel.
†
Patients aged ≥7 years receive adult Td vaccine; patients aged <7 years receive pediatric DT vaccine.
Note: Tdap (Adacel: ages 11 to 64 years; Boostrix: ≥10 years) to boost tetanus, diphtheria, and pertussis immunity can be given once
any time and then return to q 10yr schedule with Td.

Folliculitis

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I. Description

A. Superficial inflammation of hair follicles, usually due to S. aureus;

usually heals without scarring B. Scattered discrete pustules are seen at
the base of hair follicles in hairy areas (e.g., buttocks, axilla, groin, ear
canals, beard) (see color plate 12)
C. Hot tub folliculitis occurs after sitting in a hot tub; usually seen on the
buttocks, thighs, and lower trunk and is commonly caused by
Pseudomonas aeruginosa
II. Treatment

A. Hot moist compresses, antiseptic washes

B. Change razors or other personal hygiene items; if induced by a hot
tub, clean and disinfect the tub thoroughly; clean any type of exercise
mat that is used by multiple people C. Improve glycemic control
D. Topical antibiotics until lesions are healed in mild-to-moderate cases
of non-MRSA
1. Mupirocin ointment tid
2. Retapamulin ointment bid
E. Oral antibiotics if infection continues for 10 days (S. aureus may be
penicillin resistant)

Drug Pediatric Doses Adult Doses

Dicloxacillin <40 kg: 12.5-25 mg/kg/day ÷ q6h 125-250 mg q6h
>40 kg: 125-250 mg q6h
Cephalexin 25-50 mg/kg/day ÷ q12h 500 mg q12h
Clindamycin 30-40 mg/kg/day ÷ q6h 150-300 mg q6h
TMP-SMZ 80/400: 8-10 mg/kg/day ÷ q12h 160/800: 1 tab bid
Ciprofloxacin Not for children 500 mg bid (hot tub folliculitis)

III. Refer to a dermatologist if unresponsive to treatment in 2 to 3 weeks

IV. Prevention: good personal hygiene, avoid sharing personal skin care items, keep exposure to
sources of contamination at a minimum (i.e., exercise mats, showers, etc.)

Furuncle/carbuncle

I. Description

A. A furuncle (abscess) is an acute, red, hot, very tender nodule that can
evolve from folliculitis B. A carbuncle is a collection of multiple
coalescing furuncles

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 C. May have fever, malaise, and mild-to-moderate pain
D. Because of the increase in MRSA infections, treat as MRSA until
wound culture results are obtained; suspect MRSA in case of the
following:
1. Exposure at home or school
2. Recent hospitalizations or daycare
3. History of past MRSA infection
4. Abscessed wound
II. Treatment

A. Most cases resolve with warm moist compresses and if needed,

incision and drainage (I&D) (see Incision and Drainage of Abscess)
and do not require antibiotics
B. Culture the area if it is a first-time abscess
C. Improve hygiene with daily antibacterial soaps, keep fingernails clean
and short, do not share towels or personal items, change diaper
frequently for infants with abscesses D. Change all razors and do not
shave affected areas until the abscess has healed
E. Antibiotic therapy is 10 days for non-MRSA and 14 days for MRSA
infections

Drug Pediatric Doses Adult Doses Pathogen

Dicloxacillin <40 kg: 12.5-25 mg/kg/day ÷ q6h 125-250 mg q6h Non-MRSA
>40 kg: 125-250 mg q6h
Cephalexin 25-50 mg/kg/day ÷ q12h 500 mg q12h Non-MRSA
Doxycycline >8 yrs: 2.2 mg/kg q12h 100 mg q12h MRSA
Clindamycin 30-40 mg/kg/day ÷ q6h 150-300 mg q6h MRSA
TMP-SMZ 80/400: 8-10 mg/kg/day ÷ q12h 160/800: 1 tab bid MRSA

F. Refer to surgeon if unresponsive to therapy or if the symptoms worsen

G. No sports until healed, but can return to school if the wounds are
covered
H. Suggested decolonization protocol for MRSA (with recurrent skin
infections, even with adequate wound care and hygiene measures)
1. All members of the household should complete the protocol
simultaneously

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2. Mupirocin intranasally bid for 5 to 10 days monthly for up to 6 months
with or without chlorhexidine baths daily for 5 to 14 days monthly for
up to 6 months for recurrent infections (check the protocol with your
institution) 3. Dilute bleach baths for 15 minutes, twice a week for up
to 3 months (add 1⁄4c bleach to 1⁄4 bath tub of water) 4. Wash clothes in
bleach and use a hot dryer
a) clean surfaces at home with a disinfectant (1 tbsp bleach in 1 qt water)
b) improve overall hygiene of the person and the family, with focus on
hand washing

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Disorders caused by viral infections
Molluscum contagiosum

I. Description

A. A viral lesion that is a smooth, flesh-to pink-colored, raised,

umbilicated papule; may have redness or scaling around lesions (see
color plate 15) B. Lesions are considered contagious and are
transmitted by skin-to-skin contact; found anywhere on the body
(although rarely on palms or soles)
1. Face and torso are common areas in children
2. Genitals, anal area, groin, and lower abdomen are common areas in
adults
C. Generally, lesions resolve without treatment in about 6 to 12 months if
the person has a competent immune system; if immunocompromised,
lesions generally will not resolve without treatment and may be a
marker for HIV
D. Even with treatment, lesions may recur
II. Treatment

A. If inflammation is noted surrounding individual molluscum: do not

treat, this is indicative of resolution B. Surgical: curettage, cryosurgery
with liquid nitrogen, electrodessication, and laser
C. Suggested nonsurgical therapies (apply to lesions)
1. Cantharidan 0.7% topical application (painful)
2. Imiquimod 5% cream 3 times a week for 12 weeks (can be self-applied)
3. Potassium hydroxide (KOH) 10% applied bid until lesions disappear
(can be applied at home) 4. Consider topical myrtle leaf extract 1 drop
qhs until lesions disappear
D. Many sports require clearance before play
1. No play for 48 hours after curettage
2. Cover small lesions with occlusive dressing while playing

Verruca vulgaris (warts)

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I. Description: a viral lesion caused by HPV and transmitted by direct contact

A. Clinical presentation
1. Common warts are firm, small, skin-colored papules anywhere on the
body, especially on hands and feet 2. Plantar warts are thickened,
rough, skin-colored plaques found on the plantar surface of feet
B. Lesions do not itch but may be painful if in high-stress area such as the
sole of feet (see color plate 17)
II. Treatment: lesions may spontaneously resolve without any treatment

A. Surgical option with excision

B. Cryotherapy: liquid nitrogen can be used for all warts; may require
several treatments before resolution C. Flat warts may respond to
tretinoin acid cream 0.05% (Retin-A) qd with or without occlusion; can
use benzoyl peroxide 5% or salicylic acid cream 5% with Retin-A until
healed D. Plantar warts may respond to occlusive salicylic acid 40%;
keep in place for 2 to 3 days, then pare down the wart(s), and may
repeat again E. Anogenital warts may respond to imiquimod 5% cream
applied at home 3 times a week for 16 weeks F. Hand warts may
respond to cryotherapy weekly for 3 weeks
III. Refer to a podiatrist if no resolution of plantar warts

P r a c t i c e Pe a r l s f o r Wa r t T h e r a p y

• Liquid nitrogen

• When using liquid nitrogen, let the lesion thaw between treatments;
watch for a ring around the lesion to ensure adequate freezing.
• Do not use liquid nitrogen on the skin for >15 seconds at a time; if using
in children, have them count or recite letters to distract them or sing
songs during treatment.
• Duct tape can be tried over wart(s).

• Apply tape and leave on for several days, then remove the tape, pare
down the wart, and reapply the tape.

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 • May take several months, but this procedure is relatively painless.
• Another technique is to put salt compress on the wart and then apply
duct tape.
• When athletes return to play, they should cover the warts when the sport involves skin-to-
skin contact.

Erythema infectiosum (fifth disease)

I. Description

A. Initially “flulike” symptoms, followed by a red, macular blush that

looks like a “slapped cheek” and then migrates to abdomen and then
extensor surfaces of the extremities with a characteristic lacy, reticular
pattern (see color plate 23 and 24) B. The rash finally resolves but can
recur intermittently over 3 to 4 weeks, especially with exposure to
sunlight, heat/cold, or exercise C. Incubation period is 4 to 14 days; the
virus spreads via respiratory droplets
D. Patients are contagious 1 week prior to the rash but not once the rash
appears
E. Refer pregnant women to OB immediately if exposed because the virus
is fatal to the fetus
II. Treatment

A. No treatment but conservative care

B. Increase fluids to prevent dehydration
C. Use antipyretics routinely while fever is present

Roseola

I. Description

A. Common in children aged 3 months to 4 years

B. Caused by human herpesvirus 6
II. Signs and symptoms

A. Starts with high fever (up to 105°F), may have mild irritability,
rhinorrhea, and sore throat; as fever decreases in 2 to 4 days, a rose-
pink maculopapular rash appears B. The rash first appears on the
trunk and may spread to the face, neck, and extremities

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 C. The child does not appear ill; symptoms last for about 7 days
III. Treatment

A. No treatment but conservative care

B. Increase fluids to prevent dehydration
C. Use antipyretics routinely while fever is present and can use cool
sponge baths

Hand, foot, and mouth disease (HFMD)

I. Description

A. Caused by either enterovirus or coxsackievirus A16; most contagious

for the first 7 days of illness but can be infective for several weeks after
symptoms resolve
B. Transmission is by direct contact with blisters, droplets, and fecal
content (diaper changes); both adults and children can be infected C.
Abrupt onset of scattered papular and vesicular lesions found on
palms, between fingers, and on the soles of feet; oral lesions on the
soft/hard palate, buccal mucosa, and tongue may be the primary
symptom (herpangina) (see color plate 21 and 22) D. Constitutional
symptoms: fever, malaise, joint aches, and cervical adenopathy
II. Treatment

A. Self-limiting illness; usually resolves in 5 to 7 days

B. May have occasional itching
C. Use antipyretics for fever (no ASA in children)
D. Increase fluid intake
E. Treatment for mouth ulcers (herpangina)
1. OTC numbing mouthwashes or lozenges (e.g., cepacol)
2. May try diphenhydramine liquid as a mouthwash to decrease pain
3. Sucralfate (Carafate) suspension 1 g/10 ml, ½ to 1 tsp, 3 to 4 times daily
as swish and spit; this will coat and soothe the mucosa in the mouth 4.
Magic mouthwash mixture: 1 tsp swish and spit out 3 to 4 times qd,
mix equal parts of one of the following:
a) diphenhydramine + viscous xylocaine

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 b) viscous xylocaine + Maalox + diphenhydramine
c) viscous xylocaine + Maalox + prednisone liquid (can substitute
nystatin suspension) + diphenhydramine
5. Hydrocortisone 2.5 mg mucoadhesive buccal tablets placed in the
mouth near the ulcer qid after meals and allowed to dissolve slowly;
monitor for thrush

Herpes simplex (fever blisters)

I. Description

A. Infection occurs about 2 to 20 days after exposure

B. Transmitted by skin-to-skin contact with mucous membranes through
open or abraded skin or through contact with contaminated objects C.
Lesions appear as grouped vesicles, followed by erosions and
ulcerations and may appear on the lips, oral mucosa, epidermal areas,
and genitalia (see color plate 18) D. Initial outbreak may be preceded
by fever, malaise, H/A, and adenopathy
E. Subsequent outbreaks may start as a “tingling sensation,” which
indicates active infection; subsequent outbreaks have few
constitutional symptoms F. Recurrent episodes are common, especially
after stress, fever, and sun exposure
II. Treatment

A. Diagnosis is usually based on symptoms and appearance of lesions

B. Obtain viral cultures (unroof vesicle and swab fluid for best results)
C. Keep lesions moist at all times with OTC products such as Carmex or
lip balm
D. Lysine (OTC herbal product) orally or as a topical ointment, may
shorten the illness duration or lessen the intensity of symptoms
E. Topical pharmacotherapy: less effective and has to be applied
frequently for best results; apply at first sign of infection
1. OTC Abreva; apply 5 times qd; apply with a finger cot or rubber glove;
use until healed 2. Penciclovir (Denavir) cream q2h while awake for 4
days; apply with rubber gloves
3. Acyclovir 5%/hydrocortisone 1% cream (Xerese cream) applied 5 times

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 qd for 5 days
F. Pharmacotherapy for initial outbreaks should be started at the earliest
sign of infection
1. Acyclovir 200 mg 5 times qd for 5 days (adults) or 15 mg/kg ÷ 5 times
qd for 7 days (children) 2. Famciclovir 500 mg q12h for 7 days (adults
only)
3. Valacyclovir 1 g q12h for 7 days (adults only)
G. Pharmacotherapy for recurrence
1. Acyclovir 400 mg tid for 5 days, 200 mg 5 times qd for 5 days, or 800
mg q12h for 5 days (adults) 2. Acyclovir oropharyngeal MBT
(mucoadhesive buccal tablet) 50 mg (Sitavig) applied as a single dose
to the upper gum line on the same side of symptoms within 1 hour of
onset of symptoms 3. Valacyclovir 2 g bid for 2 days (adults); 2 g q12h
for 1 day (children >12 years)
4. Famciclovir 1 g bid for 1 day (adults only)
H. Pharmacotherapy for suppression (adults only)
1. Acyclovir 400 mg bid; periodically reassess the need for continued
therapy
2. Valacyclovir 500 mg qd
3. Famciclovir 500 mg bid

Herpes zoster (shingles)

I. Description

A. Discrete, vesiculopustular, grouped lesions; follows dermatomal line

(see color plate 19) B. Lesions do not normally cross the midline, but
zoster multiplex involves multiple dermatomes and possibly bilateral
distribution C. Very painful occasional itching that may precede actual
eruption
D. Postherpetic neuralgia (PHN): residual burning pain that occurs at the
site of lesions after the rash is resolved; can occur after the initial
episode of zoster and may disrupt life activities because of nerve pain
II. Treatment

A. Initiate treatment within 72 hours of outbreak (can be started as late as 5

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 days after symptoms start, but the effects may be decreased) B. Topical
comfort measures
1. Wet-to-dry dressings with sterile saline
2. Aluminum acetate topical (Domboro) solution 4 to 5 times qd
3. Calamine lotion 4 to 5 times qd
4. Zinc oxide with 0.5% iron oxide, which will help to decrease itching
and can decrease infection; also helps to dry lesions
C. Pharmacologic therapy for acute episodes (adults)
1. Antiviral agents
a) acyclovir 800 mg 3-5 times qd for 7 to 10 days
b) famciclovir 500 mg tid for 7 days
c) valacyclovir 1 g tid for 7 days
2. Other pharmacologic agents
a) steroids alone have not been proven to aid in the resolution of herpes
zoster but may improve resolution in combination with antivirals; use
40 to 60 mg qd for 7 days, then taper over 2 weeks b) pain
management with oral narcotics, acetaminophen, and/or NSAIDs
(unless contraindicated) c) amitriptyline 10 to 25 mg at hs
D. Avoid contact with immunocompromised people, pregnant women,
and people with no history of chicken pox infections E. If the
distribution involves ophthalmic nerve roots, refer to an
ophthalmologist as soon as possible because this can affect vision F.
Therapy for PHN: the goal is to prevent PHN with early treatment, but
if unsuccessful, use the following:
1. Amitriptyline 10 to 25 mg at hs
2. Nortriptyline 25 mg at hs (better tolerated at lower doses)
3. Venlafaxine 150 to 300 mg/day
4. Gabapentin 300 mg for 1 day, then 300 mg bid for 1 day, then tid
5. Gabapentin ER (Gralize) start with 300 mg and slowly increase to a
maximum of 1800 mg qd 6. Pregabalin (Lyrica) 150 to 300 mg bid
7. Tramadol 50 mg tid or an appropriate oral opiate (see Chapter 15) 8.
Topical capsaicin cream applied 5 times qd (use gloves and wash

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 hands well after use)
9. Topical lidocaine transdermal patches (lidoderm) 5% patches apply for
up to 12 hours a day in a 24-hour period; may be cut to size; no more
than three patches at a time; never reuse a patch 10. Consider TENS
unit
III. Consider referral to a pain management specialist for an epidural, stellate block, or a
sympathetic block IV. Prevention: consider varicella-zoster virus vaccine (Zostavax) for adults
aged >50 years

A. May receive even if an outbreak has occurred, but should wait until
the lesions have dried before immunizing B. Do not give if the person
is undergoing “biologic therapy” for other illnesses
C. Caution people receiving Zostavax to avoid contact for 2 weeks with
immunocompromised people, pregnant women, and children who
have not been immunized with Varivax

Varicella (chicken pox)

I. Description

A. Multi-staged papular, vesicular, pustular lesions on a red base that

crust
B. Lesions begin on the trunk and are scattered
C. Pruritus is common
D. Usually seen in young children
II. Treatment

A. Adults, elderly, or immunocompromised people need to be treated to

prevent complications
1. Varicella-zoster immune globulin (VZIG) administered as soon as
possible after presumed exposure; may be effective within 6 hours
after initial exposure 2. Protection with VZIG lasts for approximately 3
weeks; may be repeated once if reexposed >3 weeks after prior dose
B. Treatment should be started within first 24 hours after the rash starts
1. Adults: acyclovir 800 mg 4 to 5 times a day for 5 days
2. Children >2 years: acyclovir 20 mg/kg qid for 5 days (do not exceed
800 mg/dose)

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Disorders caused by fungal infection
Tinea

I. Description

A. Highly contagious, superficial, mildly pruritic infection caused by

dermatophytes
B. Well-demarcated plaques with or without pustules or papules; usually
have scaling at the edges with central clearing C. Feet may appear
macerated and show peeling, especially between toes
D. Scalp lesions can be large, with an exudate that mats hair
E. Predisposes the person to bacterial infections or dyshidrotic eczema
F. To aid in diagnosis: scrape multiple areas on the leading edge of a
lesion with a scalpel and place the scrapings on a slide; add one drop
of KOH and then heat the slide; examine under a microscope for
hyphae and spores
II. Types

A. Tinea corporis (ringworm)

1. Asymmetrically distributed, circular scaly patches with central
clearing; usually below the belt on the trunk, but can be found on the
face and torso 2. Scales are prominent on the edges of patches and are
usually associated with itching, especially in moist areas
B. Tinea capitis
1. Poorly defined, scattered areas of white scales on the head where hair
is present, with varying degrees of hair loss 2. Can be exudative under
the scales
C. Tinea versicolor
1. A cosmetic condition caused by yeast infection; usually asymptomatic
and does not itch
2. Patches or spots of hypopigmentation on the trunk, neck, and upper
arms
D. Tinea cruris (jock itch)

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 1. Pruritic, well-demarcated patches with central clearing, centered over
inguinal creases and extending down the medial thighs; in males, the
penis and scrotum are usually spared (see color plate 29)
2. Scales are seen at the periphery and may be moist and exudative or
dry with barely perceptible scale 3. Can have corresponding tinea
pedis
E. Tinea pedis (athlete’s foot)
1. Redness with maceration, fissuring, itching, and scaling; usually
between the fourth and fifth toes, sparing the dorsum of the foot, but
may have some extension on the plantar surface (see color plate 30) 2.
Occasional painful vesicular or ulcerative lesions; often, peeling of the
skin on feet and between toes
III. Nonpharmacologic treatment

A. Areas that are predominantly moist (e.g., groin, under pannus, under
breasts) should be dried thoroughly after bathing with a blow dryer if
possible B. Wear loose-fitting garments made of cotton or clothes that
are designed to wick moisture away from the body C. Avoid walking
barefoot and wear shower shoes when traveling or in communal baths
IV. Pharmacologic treatments

A. Tinea capitis usually requires systemic antifungals and antibiotics

1. Systemic (baseline testing and q4 wk while taking medication): CBC,
AST/ALT, creatinine
a) microsized griseofulvin: adults: 500 mg qd; children >2 years: 10-20
mg/kg/day qd; treatment for 4 to 6 weeks b) terbinafine (Lamisil): >40
kg: 250 mg daily; 20 kg-40 kg: 125 mg/day; treatment for 2 to 6 weeks
c) ketoconazole (Nizoral): 200-400 mg qd for 4 weeks; for children >2
years: 3.3-6.6 mg/kg qd for 4 weeks (maximum: 400 mg/dose)
2. Topical: ketoconazole 2% (Nizoral) cream or shampoo: apply 1 to 2
times qd for 2 to 6 weeks
B. Topical pharmacologic treatment for tinea versicolor
1. Selenium sulfide 2.5%: apply and leave on for 10 minutes qd for 7 to 10
days; then use monthly to prevent recurrence 2. Ketoconazole 2%
cream: apply 1 to 2 times qd for 6 weeks
3. Miconazole cream (Monistat): apply 1 to 2 times qd until resolved

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 C. Topical medications for other forms of tinea are usually effective
1. Butenafine topical (Mentax) if the patient is >12 years of age: apply to
the affected areas and surrounding skin once qd for 4 weeks for tinea
corporis, tinea cruris, and tinea pedis 2. Terbinafine (Lamisil AT):
apply bid for 1 to 4 weeks for tinea pedis, tinea corporis, and tinea
cruris 3. Ketoconazole 2% (Nizoral) cream or shampoo: apply 1 to 2
times qd for 2 to 6 weeks for tinea capitis, tinea versicolor, and others

Onychomycosis

I. Description: fungal infection of the nail bed or nail plate; can affect several digits but is more
common in toenails

A. General appearance
1. Hyperkeratotic nails with yellow-white color
2. Small, white, speckled powdery patches; nail crumbles easily
3. Milky-white discoloration of the nail plate; moves distally with nail
growth
B. Thickened toenails cause pain with poorly fitting shoes and can lead to
injury
C. May be associated with periungual inflammation, decreased
circulation, and may exacerbate venous stasis D. May interfere with
walking, balance, and exercise secondary to pain
II. Diagnostics

A. Testing is difficult; scrape under the nail or clip the nail and send to a
laboratory for analysis B. Many insurance companies will not pay for
treatment; infection must be life threatening or surgery inevitable
before coverage is approved
III. Treatment

A. This infection is not life threatening; cosmetically it is displeasing, but

keep in mind that treatment with oral medications may be more
harmful than the appearance B. Keep nails trimmed and filed
C. Tell the person to soak feet in warm water with a small amount of
cooking oil in a pan; this will soften the nails and speed clipping; after
clipping, wash feet with warm water and soap and apply moisturizer
D. Topical therapy

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 1. Ciclopirox 8% solution nail lacquer (Penlac): apply daily (the cure rate
is very low); good option for people who frequently have their hands
in water 2. Tavaborole 5% solution (Kerydin) apply daily for 48 weeks
3. Have the person fill a pan with warm water and add 1 to 2 capfuls of
bleach to 1 qt of water; soak feet in this solution for 10 to 15 minutes
bid for 2 weeks (wash feet after each treatment); the toenails will turn
white; new nails should regrow in 2 to 3 months 4. A home remedy
that has become popular is applying Mentholatum to toenails every
night until the fungal infection is resolved; may take months for results
to be seen
E. Systemic treatment (monitor liver enzymes [AST/ALT] q8 wk)
1. Terbinafine (Lamisil): 250 mg qd for 6 to 12 weeks (cure rate ∼50%)
2. Itraconazole (Sporanox): 200 mg qd for 12 weeks (cure rate ∼26%)
F. Surgical treatment to remove the nail is used as the last resort; not
proven to cure G. Lifestyle changes to prevent recurrence: avoid
communal showers, wear properly fitting footwear, treat
comorbidities (e.g., DM), prevent nail damage
IV. Refer if not responsive to treatment

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Disorders of pigmentation
Melasma

I. Description: is considered a chronic disease

A. Mostly symmetrical, macular hyperpigmentation (bronzing) in sun-

exposed areas, predominantly over the cheeks, forehead, nose, chin,
jaw angle, and above the upper lip
B. Irregular dark-brown macules and patches with well-defined margins,
seen most often in women of reproductive age with a darker
complexion; can appear with pregnancy (e.g., chloasma) C. Triggers
1. Sun (common in summer and improves in winter)
2. Initiation of OCs or HRT
3. Some antiseizure medications
4. Cosmetics
II. Treatment

A. Cosmetic treatment involves camouflaging with facial tones to hide

the darkening
B. Sun protection and sunscreens containing zinc oxide or titanium are
most beneficial and must be used for any sun exposure
III. Pharmacotherapy

A. Hydroquinone (Melanex) 3% to 4% cream: apply bid (apply a small

amount on the arms to test for hypersensitivity first); treat for 3 to 12
months B. Tretinoin (Retin-A) 0.05%: apply bid; results may be seen in
24 weeks; use sunscreen
C. Azelaic acid (Azelex) 20%: apply bid for up to 8 months
D. Fluocinolone/hydroquinone/tretinoin (Tri-Luma): apply at bedtime
E. Steroids result in initial clearing, but subsequently lead to rapid
recurrence and poor overall response

Lichen sclerosis

I. Description

168
 A. Hypopigmentation disorder resulting in loss of color, tissue thinning,
and scarring appearance; most commonly seen in the vulvar area B.
Dry, papery thin skin starting above the clitoral arch and going down
the labia majora to the perianal area (often in the shape of an “hour
glass”); does not involve the vaginal tissue C. Pruritus is severe
D. Can result in stenosis and fusion of the vaginal introitus
E. Common in older women, but can occur in children
II. Diagnostics: biopsy is indicated because it can progress to squamous cell carcinoma in 5%
cases III. Treatment

A. Avoid harsh soaps

B. Wear ventilated cotton clothes and avoid panty liners
C. Use Cetaphil as a cleanser and moisturizer
D. Use mild vaginal lubricants daily and with intercourse
E. For severe pruritus, try Domeboro solution in cool water as a sitz bath
F. Low-to high-potency steroids (see Table 5-1) for short periods of time
may relieve severe symptoms; start with bid treatment for 2 weeks,
then decrease to qd for 2 weeks, and then follow-up; treatment can be
PRN for flare-ups G. Estrogen creams may relieve symptoms (see
Table 11-4)
IV. Refer to a dermatologist or gynecologist for persistent symptoms

Vitiligo

I. Description

A. Discrete areas of the skin and mucus membranes are depigmented;

the most commonly affected sites are as follows:
1. Dorsal hands and arms
2. Body creases and genitalia
3. Orifices of the mouth, face, neck scalp, anus, and nose
B. Tends to occur between 10 to 30 years of age and can be progressive
C. May be associated with the following conditions:
1. Alopecia
2. Thyroiditis, Graves’ disease

169
 3. Pernicious anemia
4. IBS, psoriasis, type 1 DM
II. Treatment: no permanent cure, and resolution with treatment is less than optimal
III. Refer to a dermatologist

Acanthosis nigrans

I. Description

A. Symmetrical, thickened, darkened areas of skin that feel “velvety” and

are located in body creases (e.g., axilla, neck, and groin; also face,
elbows, knees, and hands) B. Three types
1. Type 1: associated with malignancy (e.g., especially stomach and lung)
2. Type II: familial and is seen at birth
3. Type III: associated with obesity, insulin resistance disorders,
Cushing’s disease, Addison’s disease, and hyperandrogenic and
hypogonadal states
C. Can be caused by certain medications such as steroids, OCP, insulin,
and testosterone
II. Treatment

A. Treat the cause

1. Control endocrine disorder
2. Lose weight
3. Medication consideration: metformin (see Metabolic Syndrome in
Chapter 16), topical retinoic acid or salicylic acid (see Table 5-5), and
fish oil
B. Laser treatments may correct discoloration
III. Refer if unresponsive to treatment or if malignancy is considered

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Skin lesions
Skin tags

I. Description

A. Flesh-colored, soft, and pliable papilloma with a stalk; occurs

anywhere on the body, but mostly in intertriginous areas
B. Varying sizes; small at the base (<1 mm up to 10 mm)
C. Causes cosmetic disfigurement and discomfort at the site because of
friction; is not usually malignant
II. Treatment

A. Remove by snipping off with a sharp scalpel or scissors, cryotherapy,

or punch biopsy
B. Send to pathology if indicated

Epidermoid cyst

I. Description

A. A slow-growing subcutaneous cyst that is smooth and usually

nontender
B. History of intermittent drainage with a purulent discharge
1. Has a small central punctum (core) that differentiates it from lipoma
(see color plate 3) 2. Cyst contents, when present, are usually cream-
colored with a cottage cheese–like consistency and foul odor
C. Can be small (0.5 cm) to large (5 cm); usually a solitary nodule
D. Can become inflamed with persistent irritation
II. Treatment is incision, drainage, and removal of the sac

Actinic keratosis

I. Description

A. Premalignant lesions usually caused by sun exposure, with an

increased risk for squamous cell carcinoma (SCC) B. Lesions are
symmetrical and have scaly appearance (see color plate 25) C. Usually

171
 have been present for a long time as a chronic scale that can be
scratched off but will always come back without treatment
II. Treatment

A. Cryotherapy
B. Curette excision
C. Can use imiquimod for multiple lesions
D. Lesions that do not respond require surgical removal and pathology
III. Refer to a dermatologist if a large area of the skin is involved, if the lesion returns after
therapy, or if there are concerns for cancerous changes

Keratocanthoma

I. Description

A. Lesions are symmetrical and dome shaped, with a central plug and
crust; borders are smooth, well demarcated; nodule is firm and not
painful B. The lesion grows rapidly and may double within a 2-week
period up to 2 cm in size; in contrast, basal cell carcinoma or squamous
cell carcinoma is more “slow” growing and may take months to years
to double in size C. Found primarily on sun-exposed areas such as the
face and extremities
II. Treatment

A. Cryotherapy for smaller lesions

B. Deep shave or conventional excision with free margins; send to
pathology
C. Can recur; monitor the area after treatment every month for 3 months
III. Refer if resistant to treatment.

Basal cell carcinoma (BCC)

I. Description

A. Lesions are usually round with small central ulcerated depressions on

a pearly raised base. Borders are smooth with increased vascularity
around the rim (see color plate 26) B. Can be nonhealing or recurrent,
irregularly shaped, and bleeds easily
C. Color variation: from pale white to pink, flesh-colored to red, but can

172
 be darker in color D. Usually develops on sun-exposed skin in middle-
aged, fair-skinned people with significant outdoor exposure E. Does
not usually metastasize, but has an increased rate of recurrence,
especially in nasolabial folds and preauricular areas
II. Treatment

A. Any nonhealing lesion should be biopsied

B. Remove smaller, superficial lesions with cryotherapy or punch biopsy
C. Remove lesions >1 cm or facial lesions with surgical excision or refer
to a dermatologist
III. If the lesion is >10 cm, in an area of high recurrence (nasolabial fold), or recurrent after
treatment/removal, refer to a dermatologist

Squamous cell carcinoma (SCC)

I. Description

A. Nonhealing lesions that are slightly raised with scaling, having

irregularly shaped, sharply demarcated borders (see color plate 27)
1. May be ulcerated, with a crust in the center on a firm, moveable base
2. Usually found at the base of actinic keratosis
3. Diameter varies
B. Found mainly on sun-exposed areas
C. More aggressive than BCC and can metastasize into surrounding
areas
II. Treatment

A. Smaller lesions can be treated with cryotherapy with attention to

recurrence
B. Consider biopsy of lesions for confirmation
C. Can use imiquimod 5% until the lesions resolve
III. Refer to a dermatologist or surgeon

Melanoma

I. Description: all lesions vary; use the following mnemonic for assistance in identifying
abnormal skin lesions (see color plate 28)

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A = Asymmetry, such as a lumpy, bump-on-bump appearance
B = Border irregularity, such as a scalloped, cauliflower, or spreading
pattern
C = Color variation, such as two or more colors present in the lesion (e.g.,
red, white, blue, brown, or black)
D = Diameter >0.6 cm (approximately the size of a pencil eraser); growth
either vertically (indicated by puckering of the surrounding skin [poor
prognosis]) or horizontally E = Evolving/elevating lesion that was
previously flat, change in texture, dimpling, or itching
II. Risk factor: family history or recurrent personal history of melanoma
III. Treatment: urgent referral to a dermatologist or surgeon

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Wound care

P r a c t i c e Pe a r l s f o r B u r n s

• Superficial burns should be gently cleaned with cool water and plain soap.

• Apply cool compress; should heal in 3 to 7 days.

• May try aloe gel (plain), aloe gel with xylocaine, or aloe gel spray for
pain relief.
• Second-degree burns usually blister; keep covered with a nonstick dressing and possibly
silver sulfadiazine (Silvadene) and do not attempt to break open the blisters; change the
dressing twice daily.
• Minor burns are painful; use acetaminophen 500 to 1000 mg tid or ibuprofen 400 to 800 mg
tid (see Tables 17-2 and 17-3 for child doses).
• Tar burns can cause deep tissue injuries because of continued burning until removal; use
mayonnaise or mineral oil to remove tar.
• Consider tetanus prophylaxis (Table 5-6).
• Refer the following burns:

• Circumferential burns; burns involving the face, chest, or neck; or

burns in children with a poor and concerning history of injury or burn
pattern • Burns of a severity greater than second degree and/or
involving the fascia and tendons, ligaments, or muscle • Electrical
burns

Minor abrasions, scratches, superficial lacerations

I. Clean the area thoroughly with soap and water

II. Keep covered with a clean, dry bandage while working; may remove at night
III. Consider using OTC or prescription antibiotic ointments or petroleum jelly to prevent
sticking; do not use ointments with Neosporin as this can cause tissue irritation IV. May need to
use a butterfly dressing for a small, superficial laceration to hold the edges together V. May use
Dermabond with a simple, clean laceration that is easily approximated
VI. Ask about tetanus prophylaxis (see Table 5-6)

Human bites

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I. Clean thoroughly with soap and water, followed by irrigation with normal saline
II. Ask about tetanus prophylaxis (see Table 5-6)
III. Oral antibiotics are given for 10 days:

Drug Pediatric Dose Adult Dose

Amoxicillin/clavulanate <3 mos: 30 mg/kg/day ÷ q12h 500/875 mg q8-12h
>3 mos, <40 kg: 25-45 mg/kg/day ÷ q12h
Cephalexin 25-50 mg/kg/day ÷ q12h 500 mg q12h
Clindamycin 30-40 mg/kg/day ÷ q6h 150-300 mg q6h
Levaquin Not recommended for children 500 mg qd

IV. Use hot moist soaks or hot packs minimum of qid

V. Monitor for cellulitis; recheck in the office at least once within the first 24 hours regardless of
the size of the bite VI. Do not suture human bites

Punch biopsy

I. Can easily remove small skin lesions and embedded ticks; can facilitate obtaining a sample for
pathologic examination II. After anesthetizing and prepping the skin, stretch the skin around the
lesion 90 degrees to the proposed direction of the linear closure III. Lightly depress the
instrument over the lesion while turning it; remove the instrument and release skin tension IV.
Excise the cored-out lesion from the punch; the resulting incision should be an ellipse that can be
easily sutured V. Suture with respect to skin lines to decrease scar formation

Lacerations and suturing (table 5-7)

I. Description

A. Methods for primary closure of wounds within 8 hours of injury

(except on the face and scalp) include sutures, Steri-strips, staples, and
Dermabond B. Secondary closure/healing involves allowing the
wound to close on its own; the wound must be cleansed very well and
debrided if necessary; assess “dirty” wounds more frequently during
the healing process; a Penrose drain can be placed to facilitate drainage
II. Use of anesthesia

A. Before using a local anesthetic on the wound, drizzle/spray a small

amount into the laceration to decrease some of the pain when
infiltrating B. Anesthetize the wound using the smallest needle
possible (e.g., 27 gauge); inject slowly into the wound edges, not into
the intact skin; inject each side of laceration with as few punctures as
possible C. Digital blocks work well for providing anesthesia in finger
and toe wounds/lacerations

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 D. Never use an anesthetic with epinephrine in or on fingers, toes, ears, nose,
penis, or any area with poor vascular supply
III. Suture points to consider when repairing wounds (see Table 5-7)

A. Before suturing lacerations that involve the extremities, assess the

distal digits’ neurovascular status (i.e., sensation, strength, and
movement)
B. Assess the degree of wound tension by observing the wound edges; if
the edges are close with minimal tension, a good cosmetic closure will
result C. If the edges are >5 mm apart, there is increased tension and
the wound should be repaired in layers for best results D. When
removing a lesion, make the incision parallel to the skin tension lines;
this will decrease scarring (gently pull the intact skin in different
directions to see which way the natural line of the skin moves) E. To
check wound thickness, use the stick end of the applicator and set into
the injury; if it will not drop through the skin, consider partial
thickness F. After the wound is anesthetized, clean vigorously and
irrigate profusely (the cleaner the wound, the less likely that infection
will occur). Do not suture highly contaminated wounds, human or
animal bites, wounds older than 24 hours, or puncture wounds.
IV. Postwound care

A. Wound care rechecks should be done in 24 hours for contaminated

wounds, in 5 to 7 days for “clean” wounds, and before removing
sutures B. Instruct the person to keep the wound dry and clean; if the
dressing accidentally becomes wet, change the dressing immediately
C. Have the person (or caregiver) gently clean the edges of the wound
daily with a cotton swab saturated with peroxide to remove crusts
(this will decrease scarring by facilitating the healing of wound edges)
D. Caution the person to return immediately if signs of infection occur
1. Redness or red streaks progressing up an extremity
2. Increasing pain
3. Swelling
4. Fever
E. Use broad-spectrum oral antibiotics for lacerations with the following:
1. Traumatic injury and contamination

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 2. Untidy wounds and inadequate debridement
3. Joint wounds
4. Wounds >6 to 12 hours old
5. Animal and human bites
6. Compromised host
V. Ask about tetanus prophylaxis (see Table 5-6)

Table 5-7
Suture Points

Suggested Suture
Suture Removal
Size
Deep
Location Skin Adult Child
Absorbent
Scalp 4-0, 4-0 6-7 days 5-6 days
5-0
Face or 6-0 5-0 4-5 days 3-4 days
forehead
Eyebrow 5-0, 5-0 4-5 days 3-4 days
6-0
Lip, nose, or 6-0 5-0 (n/a for 4-5 days 3-4 days
ear ear)
Trunk 4-0, 3-0 7-10 days 5-9 days
5-0
Arm or leg 4-0, 3-0 Joint spared: 7-10 days Joint spared: 5-9 days
5-0 Joint (extensor surface): 8-14 Joint (extensor surface): 7-12
days days
Joint (flexor surface): 8-10 Joint (flexor surface): 6-8
days days
Hand 5-0 5-0 Dorsal: 7-9 days Dorsal: 5-7 days
Palm: 7-12 days Palm: 7-10 days
Plantar foot 3-0, 4-0 7-12 days 7-10 days
4-0

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Incision and drainage (I & D) of an abscess
I. Description

A. An abscess (furuncle or carbuncle) is a localized infection with an

encapsulated collection of pus surrounded by inflamed skin B. Usually
caused by S. aureus, MRSA, or streptococci
C. Abscesses can occur anywhere on the body
II. Guidelines

A. For a small, localized abscess, start with hot, moist compresses; this
may be adequate treatment for the body’s defenses to clear the
infection with or without oral antibiotics (antibiotics are usually not
required after I&D) B. If an abscess enlarges or starts to drain but has
inadequate core opening, then I&D will be required
1. An abscess is “ready” to be incised with good results if the central
portion of the abscess is “soft” to touch (e.g., feels like the tip of your
nose), but the surrounding skin may stay firm 2. The area is usually
“under pressure,” so beware of injecting local anesthesia and during
the first incision—either of these procedures may produce an eruption
of purulent material that could “erupt” up to one foot!
III. Steps to I&D

A. Gently scrub the entire inflamed, abscessed wound area with

antibacterial soap and water B. Swab with betadine or alcohol (if
allergic to iodine)
C. Inject a local anesthetic (xylocaine with or without Epi) around the
tissue perimeter to avoid the central cavity; it is difficult to completely
anesthetize a large abscess D. Can also use topical spray anesthesia
such as ethyl chloride
E. Incision is made using a #11 scalpel through the center of the abscess
following skin lines
1. The purulent material should be easily expressed (and may “squirt”
out)
2. The incision does not have to be as wide as the abscess
3. If culturing, use a sample of the expressed purulent material and not of

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 the superficial skin
F. Use external pressure to express the purulent material
G. Using hemostats, explore the cavity for pockets of pus and to find any
tunneling of the abscess through soft tissue
1. Occasionally the abscess opening is NOT located over the center of the
abscess. This may need to be referred for further surgical exploration.
2. For epidermoid cyst, try to remove the cyst sac to prevent recurrence
H. Irrigate the abscess with copious amounts of sterile saline or half
saline and half hydrogen peroxide I. Consider packing the wound with
an adequate amount of iodoform gauze and leave a “tail” of the gauze
outside the wound for easy retrieval at next dressing change J. Apply
ointment over the gauze to prevent the “tail” from sticking to the
overlaid dressing
IV. Postwound care

A. Can continue warm packs over dressing tid

B. Change packing q2-4d but change the outer dressing more often,
depending on the amount of drainage from the abscessed wound C.
The amount of packing needed should gradually decrease with each
packing change; monitor for decrease in the redness and size of the
wound D. If the wound continues to drain and apparent infection is
noted, start oral antibiotics

Drug Pediatric Dose Adult Dose

Dicloxacillin <40 kg: 12.5-25 mg/kg/day ÷ q6h 125-250 mg q6h
>40 kg: 125-250 mg q6h
Cephalexin 25-50 mg/kg/day ÷ q12h 500 mg q12h
Clindamycin 10-25 mg/kg/day ÷ q6h 150-300 mg q6h
Ciprofloxacin Not to be used in children 250-500 mg bid

E. If unresponsive to antibiotic therapy after 3 days, refer to a surgeon

F. Recurrence of an abscess in the same location is usually due to inadequate incision and/or
premature wound closure

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Things that bite and sting
Rattlesnake, water moccasin, and copperhead bites

I. Be calm and keep the victim calm

II. Remove any constricting jewelry/clothing
III. Note the amount of time between the bite and appearance of symptoms if available
IV. Keep the affected extremity below heart level
V. Transport to the ED for further care

Domestic animal bites

I. Guidelines

A. Bites are usually related to cats or dogs

B. If the child is <2 years old and has facial or scalp wounds, refer to ED
C. Infection risk is highest on hands or with puncture wounds and crush
injuries
II. Treatment

A. Tetanus prophylaxis (see Table 5-6)

B. Anesthetize the wound and cleanse thoroughly with copious amounts
of antibacterial soap C. If the wound is >8 hours old, consider culture
of the wound site
D. Debride the devitalized or necrotic tissue—except on the face
E. Use mupirocin ointment and bandage with a clean dressing daily;
wound closure is not recommended F. Splinting of the extremity may
aid in healing
G. Systemic antibiotics for 10 days

Drug Pediatric Dose Adult Dose

Amoxicillin/clavulanate <3 mos: 30 mg/kg/day ÷ q12h 500/875 mg q8-12h
>3 mos, <40 kg: 25-45 mg/kg/day ÷ q12h
Dicloxacillin <40 kg: 12.5-25 mg/kg/day ÷ q6h 125-250 mg q6h
>40 kg: 125-250 mg q6h
Cephalexin 25-50 mg/kg/day ÷ q12h 500 mg q12h
Clindamycin 10-25 mg/kg/day ÷ q6h 150-300 mg q6h

H. Follow the state laws for reporting animal bites

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 I. If there is no record of rabies vaccination for the offending animal or if
the animal cannot be quarantined and the risk is high, consider rabies
immune globulin (RIG) and 5 days of rabies vaccine J. Follow-up in the
office in 24 hours to evaluate the wound
III. Refer to ED if the infection is not improving in 24 to 48 hours

Feral or wild animal bites

I. Rabies

A. Carriers
1. Principle carriers of rabies: bats, foxes, raccoons, skunks, coyote,
cats/dogs
2. Rarely carry rabies: squirrels, mice, rats, rabbits
B. Signs and symptoms
1. Symptoms of rabies may not appear for up to 10 days; bat bites may go
undetected because of the size of the bite area and the painless act of
biting 2. Initial symptoms include the following:
a)  H/A, jaw pain
b) photophobia; dizziness
c) numbness
d) fever, N/V
3. As the disease progresses, symptoms include changes in cognition and
gait disturbances
4. Final stage of the disease is cardiovascular collapse
C. Treatment
1. Tetanus prophylaxis (see Table 5-6)
2. Individuals who have been attacked by wild animals carrying an
increased risk of rabies should have postexposure prophylaxis; the
animal should be tested, if possible 3. Consider rabies immune
globulin (RIG) infiltration directly into the exposure sites depending
on the weight; if there is excess RIG, give remaining RIG IM
4. After RIG is given, follow with 4 days of rabies vaccine (HDCV) if the
person is immunocompetent or 5 days if immunocompromised

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 a) do not use IM RIG in the same muscle site as rabies vaccine
b) if the animal in question is subsequently tested and no rabies is found,
then treatment can be stopped
5. Wound care
a) if wound is on face, refer to plastic surgeon or ED
b) Thoroughly cleanse the wound after anesthetizing with copious
amounts of sterile saline (can prevent up to 90% of rabies
transmission) c) debride the necrotic tissue (except on the face)
d) wound closure with glue, adhesive strips, or sutures can be
considered (after RIG infiltration into the wound site) when there is a
low risk of infection; otherwise, closure is discouraged
D. Follow the state laws for reporting animal bites

Tick-borne diseases

I. Lyme disease

A. Description
1. Most common tick-borne disease caused by Borrelia burgdorferi; occurs
more often in late spring and summer months 2. Incubation period is 7
to 10 days
3. There is increased risk of transmission if the tick is attached for >24
hours
B. Signs and symptoms (may not appear for 30 days)
1. Stage I symptoms
a) erythema migrans
b) fever; malaise; myalgia
c) lymphadenopathy and H/A
2. Stage II symptoms are the same as above and include the following:
a) migratory arthritis
b) Bell’s palsy
c) asymptomatic first-degree AV block
d) myocarditis (rare)

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 3. Stage III symptoms are the same as those for Stage I and II and include
the following:
a) scleroderma-like lesions on knees and elbows
b) severe fatigue, sleep disorders, and confusion
c) paralysis and cranial nerve defects
C. Treatment
1. Diagnosis is difficult because of unreliable testing
2. Supportive care with rest, hydration, and NSAIDs for pain
3. Early intervention with oral antibiotics may prevent adverse effects

Adult Dose for 14-21

Drug Pediatric Dose for 14 Days
Days
Doxycycline >8 yrs, <45 kg: 4 mg/kg/day bid for 1 day, then 2.2-4.4 100 mg bid
mg/kg/day ÷ q12h
Amoxicillin >3 mos, ≥40 kg: 50 mg/kg/day ÷ q8h 500 mg tid
Cefuroxime 3 mos to 12 yrs: 30 mg/kg/day ÷ q12h 500 mg bid

4. Can use macrolides if allergic to these antibiotics, but they are less
effective
5. For more severe symptom management, refer to an infectious disease
specialist
II. Rocky Mountain Spotted Fever (RMSF)

A. Description
1. Tick-borne disease caused by Rickettsia bacteria
2. Infection found predominantly in Southeast and Midwest United
States and commonly occurs from April to September 3. Transmission
occurs within hours of the bite and symptoms occur within 2 to 10
days
a) symptoms occur suddenly with fever, headache, and rash (classic
triad)
b) initially a blanching pink macular rash appears on the ankles, wrists,
and forearms; the rash then becomes maculopapular and spreads to
the trunk
B. Diagnostic testing

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 1. Always ask about travel history and tick exposure
2. Diagnosis relies on heightened suspicion, predominance of endemic
area, and season of the year 3. CBC may show a normal or low
leukocyte count with a left shift, decreased RBCs, decreased platelets
C. Treatment is referral to ED if RMSF is suspected
III. Ehrlichiosis

A. Description
1. Tick bites frequently occur from May to August and transmission
occurs immediately after the bite 2. Signs and symptoms occur within
7 days of exposure
a) at onset, the symptoms include fever, chills, H/A, myalgia, and
malaise
b) later, N/V, anorexia, and weight loss occur
c) petechial, maculopapular rash and edema in the hands and feet are
more common in children d) adults more likely to have cough,
confusion, and lymphadenopathy
3. Can progress to renal failure, meningoencephalitis, coagulopathy, GI
hemorrhage, pulmonary complications
B. Laboratory values
1. Thrombocytopenia (50,000/µL to 140,000/µL, but can be <20,000/µL)
2. Mild-to-moderate leukopenia (neutropenia and lymphopenia)
C. Treatment
1. Diagnosis is based on suspicion of the disease and history of tick bites
before symptoms appeared 2. Ehrlichia organisms are resistant to most
antibiotics and therapy is limited to doxycycline bid for 7 to 14 days
a) adult dose: 100 mg
b) child dose: <45 kg (e.g., 100 lb): 2.2 mg/kg bid
3. Supportive treatment for other symptoms
D. Refer to ED if there are significant symptoms

Spider bites

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I. Brown recluse spider bite

A. Description: not an aggressive spider; likes dark, little-used areas;

bites usually occur when the spider is caught in clothing or bed linens
B. Signs and symptoms
1. Within 1 to 24 hours after the bite, the patient complains of “pin-
pricking” sensation followed by irritation, itching, and redness 2. After
24 hours, the site of bite turns deep blue-purple, surrounded by a
white ring and a large outer ring; may be raised or bullous; will be
painful 3. After 48 hours, the site will develop ulceration in the center,
which will gradually enlarge and slough 4. May experience H/A, body
aches, rash, fever, and N/V
5. Wounds are usually worse if they occur in highly adipose tissue
C. Treatment
1. Cleanse the area thoroughly
2. Use an antibiotic ointment or oral antibiotics for secondary infection
3. Apply ice packs
4. Use NSAIDs or acetaminophen for pain
5. Conservative wound care; there is no specific treatment for bite
wound; not all bites progress to tissue sloughing 6. Refer to a surgeon
if the lesion is enlarging and sloughing
7. Td prophylaxis if indicated (see Table 5-6)
8. Antihistamine for any itching
9. Hyperbaric oxygen therapy may have positive benefits to aid in
healing without surgery or after surgery to assist in wound healing 10.
Ineffective therapies (no proven benefits)
a) dapsone has been tried to slow the sloughing process
b) nitroglycerin patch has been tried to increase circulation to the ulcer
by applying over the wound c) steroid injections into the site have
been tried with little success
II. Black widow spider bites

A. Description: slightly aggressive spider; lives in dark, secluded places

such as wood piles and barns (close, dark areas); majority of the bites
occur in summer B. Symptoms may not occur immediately after the

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 bite, but the person will complain of severe pain, burning, redness, and
swelling at the site followed by more severe symptoms within 1 to 12
hours
1. H/A, dizziness
2. Itching with rash that can be localized to the bite location or spread
into the region of the bite 3. Restlessness, anxiety, and sweating
4. Dysautonomia symptoms (i.e., eyelid edema, ptosis, HTN, salivation,
weakness, N/V)
5. Intractable pain with rigid muscles in the abdomen, back, and chest
6. Muscle tremor, fasciculations, cramping, and leg pain in major muscle
groups
7. Symptoms can last from a few hours to a few days from the time of the
bite
C. Treatment
1. Treatment is usually supportive with local wound care
2. Application of ice to the bite area
3. Significant analgesia may be needed along with benzodiazepines to
relieve anxiety
D. Refer to ED with life-threatening symptoms

Mosquito-borne diseases

I. West Nile virus (WNV)

A. Description
1. The disease is spreading throughout United States
2. The illness can be very mild, similar to “cold” symptoms lasting about
3 to 6 days, or can be very severe (lasting weeks), leading to death;
incubation period is 3 to 14 days
B. Signs and symptoms
1. May include acute febrile illness followed by the following:
a) malaise, myalgia, anorexia with N/V
b) headache, eye pain

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 c) rash, lymphadenopathy
2. May progress to severe neurological disease with encephalitis, ataxia,
seizures, and neuritis
C. Treatment
1. Diagnosis is based on positive IgM antibody to WNV in the serum or
spinal fluid
2. Antipyretics, analgesics, rest, and hydration
3. This is a reportable illness; notify the local health department
D. Prophylaxis: mosquito control by draining all standing water,
cleaning out drains, and removing all items that might hold water; if
going outdoors at night, use mosquito repellant with DEET and wear
long sleeves E. Refer to ED with unresolving respiratory infection or no
response to treatment in 24 hours
II. Malaria

A. Description
1. The disease is a major problem for world travelers
2. Symptoms usually occur 7 to 9 days after exposure
B. Signs and symptoms
1. Cyclic fever and shaking chills
2. H/A
3. N/V/D, abdominal pain, splenomegaly, bloody diarrhea
4. Muscle aches, back pain
5. Jaundice, dark urine
C. Diagnosis
1. Diagnosis can be made from a history of recent visit to an endemic
tropical area
2. Blood smear for plasmodium species is confirmative; if positive, refer
to an infectious disease specialist
D. Prevention and treatment
1. Consult the CDC website (www.cdc.gov) for information on prevention
according to the country of travel and prophylactic treatment before

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 traveling 2. Preventive treatment depends on the destination;
medication should be started before traveling to endemic countries 3.
Use an insect repellant on all exposed skin areas whenever outdoors;
use mosquito netting and avoid going outdoors between dusk and
dawn

Parasitic infestation

I. Bed bugs

A. Description
1. #1 urban pest; incidence has increased since the banning of DDT
2. Transmission occurs when bed bugs attach to personal belongings
(e.g., luggage, clothing, furnishings) and travel to home or the next
destination 3. Bed bugs are small, blood-sucking insects that hide
during the day and come out at night 4. Bites cause allergic reactions to
the insect’s saliva, but there is no known transmission of disease to
human hosts. The bugs feed on humans but do not live on the skin.
B. Signs and symptoms
1. The chief complaint is intense itching and mild skin inflammation with
erythematous maculopapular (often) clustered lesions, which are
usually found on the head, neck, and upper body, especially around
the elastic portions of clothing 2. Mild reactions include small,
maculopapular erythematous lesions at the feeding site within 72
hours of exposure; if not scratched, will resolve after ∼1 week 3.
Moderate -to-severe reaction includes wheals, diffuse urticaria, blood
blisters; reaction continues as long as exposure remains; can have
occasional systemic reaction with angioedema 4. Insomnia (from
itching)
5. Emotional distress secondary to thought of infestation
C. Treatment
1. Remove infestation
2. Wash everything with soap and water
3. Topical application of OTC pramoxine, doxepin cream, or intermediate
steroid ointment
4. If infection appears (usually from scratching), use mupirocin ointment

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 5. Oral antihistamines (e.g., hydroxyzine or diphenhydramine) can be
used at night to decrease the “itch-scratch” cycle
II. Pediculosis capitis (head lice)

A. Description
1. Head lice is a common infestation by a small parasite called Pediculus
humanus capitis 2. Found worldwide; is most common in children aged
3 to 12 years
3. Transmission occurs when hats, combs, hairbrushes, and caps are
shared; lice are spread through direct contact
B. Signs and symptoms
1. The adult louse is small, grayish in color and very agile; it is
approximately 3-mm long with six legs 2. The scalp is the most
commonly affected area, but the louse can inhabit the eyelashes,
eyebrows, and beard 3. Nit infestation is most commonly found
behind the ears, on the nape of the neck, and on the crown of the head;
nits are usually located near the hair shaft and are usually of dark
color; as the nits hatch, the casing turns white and is easier to see (see
color plate 31) 4. In many areas of United States, resistance is
developing to standard medications used for treatment
C. Treatment
1. Should always involve removing the nits; this can be time consuming,
and many parents will not take the time to remove all nits; shaving the
head is an easy treatment for boys, but not for many girls; instruct the
parent to use bright light and several hair clips and section off the hair
for easier identification of nits; nit combs may miss nits but will
remove actual lice—use q2 to 3 days to decrease reinfestation 2. Some
hair rinses will facilitate nit removal by loosening the nits attachment;
try a vinegar and water rinse 3. All head lice preparations are applied
at bedtime after washing the hair, and a shower cap can be worn to
increase the effectiveness of the product; prevent the product from
entering the eyes or mouth; rinse it out in the morning; retreat only if
live head lice are present 4. Tea tree oil can be used daily and may
eliminate live head lice; nits still have to be removed manually 5. First-
line OTC topical head lice preparations for anyone >2 years and can be
reapplied in 9 to10 days if needed; these preparations do not kill the
nits

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 a) permethrin 1% cream rinse (e.g., Nix etc.)
b) pyrethrin 0.3%/piperonyl butoxide (e.g., Rid, etc.) 3% to 4% liquid, gel,
or shampoo
6. Topical preparations for resistant head lice
a) malathion 0.5% lotion (e.g., Ovide) applied once and can retreat in 7 to
9 days; approved for children aged >6 years b) benzyl alcohol lotion
5% (Ulesfia) applied once and can retreat in 7 to 9 days; approved for
infants aged >6 months c) ivermectin lotion 0.5% (Sklice) single 10-
minute application, approved for infants aged >6 months d) spinosad
topical suspension 0.9% (Natroba) single application and may repeat
in 7 days if live lice are found; approved for children aged >4 years
7. Oral head lice medications for resistant head lice
a) bactrim 5 mg/kg bid for 10 days; works best if used with Nix shampoo
b) ivermectin 200 mcg/kg (Stromectol) initially and repeated in 7 days;
approved for children weighing >15 kg
8. Environmental cleaning must be started with other treatments
a) wash all clothing worn over the last 3 days in hot water (130°F) and
dry for 20 minutes on hot cycle in a dryer b) store nonwashable items
in a closed plastic bag for 2 weeks
c) vacuum the floor and furniture where the person sat or lay
III. Sarcoptes scabiei (scabies)

A. Description: scabies is a skin infestation caused by a mite and is

spread by close contact B. Signs and symptoms
1. Nocturnal itching is the presenting symptom
2. Primary lesions are papules with burrows, but vesicular lesions
without burrows may be present 3. In adults, the scalp, face, and upper
back are spared; in infants, these areas are not spared, and lesions may
be found on palms and soles 4. Burrows are common between the
fingers, flexor areas of the wrist, penis, vulva, nipples, axilla, and
buttocks; vesicles can be found on the sides of fingers (see color plate
16)
C. Treatment
1. Pharmacologic therapies

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 a) permethrin 5% cream (Elimite): apply to the skin from the neck down,
leave on for 8 to 12 hours, and then wash off; may repeat once in 7
days; approved for infants aged >2 months b) crotamiton (Eurax) 10%
cream/lotion: apply from the neck down, leave on for 24 hours, and
then wash off; repeat in 24 hours; approved for adults only c) lindane
1% cream: apply to the skin from the neck down, leave on for 6 hours,
and then wash off; the patient may repeat treatment in 1 week;
approved for adults weighing >110 lbs; not approved for children or
pregnant women d) ivermectin 200 mcg/kg orally once, repeat in 2
weeks; approved for children weighing >15 kg and for adults; not
approved for pregnant women
2. Treat all close contacts; wash all linens and clothes in hot water (130°F)
and dry on hot cycle in a dryer; for nonwashable items, store in a
tightly closed plastic bag for 2 weeks 3. The patient may need
antihistamines for itching, which may continue because of increased
sensitivity to dead mites and mite by-products 4. If itching continues
for >7 days, consider retreatment; however urticaria may last for
several days after treatment because of the allergic components of the
infestation. Use topical steroid creams to help with local inflammation.

Stinging injuries

I. Bee stings (hymenoptera)

A. Description
1. Non-Africanized bees sting only once and never in swarms
2. Africanized bees can sting multiple times and in swarms
3. Venom is protein based and has a high risk for causing allergic
reactions that can be lethal in sensitive people
B. Signs and symptoms
1. Local reactions: pain at the site with redness, edema, and pruritus
2. Systemic reactions: pain at the site with N/V, syncope, wheezing, H/A,
seizures, hypotension, muscle spasms, cardiopulmonary arrest 3. No
correlation between the number of stings and allergic reaction
4. Can have delayed serum sickness 10 days after being stung
C. Treatment

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 1. Local treatment involves removing the stinger, if possible by scraping
with a card or similar object 2. Apply ice to the area
3. Use OTC antihistamines and NSAIDs routinely q6h for the first 24
hours
4. If the person has a more severe reaction, consider using epinephrine
SQ 0.1 to 0.5 ml of a 1:1000 solution and IM or oral corticosteroids 5.
Transfer to ED if the symptoms are not resolving quickly or if
respiratory distress has occurred
D. Prophylaxis: prescribe self-administered EpiPen and encourage the
person to obtain a Medic Alert bracelet
II. Fire ant stings

A. Description
1. An aggressive ant that resides in southern states, lives in underground
burrows, and swarms victims when the anthill is threatened; each ant
can sting numerous times 2. The site of sting is immediately painful
with a burning sensation, followed by development of a vesicle that
will progress to a pustule and can cause tissue necrosis and superficial
scarring 3. Extreme pruritus follows
4. Generally localized symptoms with multiple stings; systemic reactions
may be seen; stings are more severe in young children
B. Treatment
1. Monitor for severe systemic allergic reactions and transfer to ED if
present or if a child is attacked
2. Supportive treatment with ice and elevation of the extremity
3. Immediate application of a moistened meat tenderizer to the bite may
decrease local reaction 4. Antihistamines (e.g., diphenhydramine) for
pruritus
5. Topical steroids (e.g., triamcinolone, desoximetasone) to the sting
areas; may need a brief course of oral prednisone 6. Monitor for
infection at the site(s)
C. Prevention
1. Wear shoes and avoid anthills or regions where ants are commonly
found; monitor young children closely 2. To keep anthills away from

193
the house, use approved chemicals to dispense on lawns or in fire
anthills

194
CHAPTER 6

195
Respiratory conditions
For details regarding complete history and physical examination, see Chapters 1 and 2.

Specific tests for assessing pulmonary function

I. Pulse oximetry

A. A noninvasive method of estimating and monitoring oxygen

saturation in the blood B. Normal is >92%
II. Peak expiratory flow rate (PEF) (see Table 6-1 for the PEF chart)

A. Reflects large airway flow; it is decreased in obstructive diseases and

with age B. Normal is >80% predicted
C. May be used in office or at home to monitor the effects of treatment
and the status of the disease process
III. Pulmonary function testing (PFT)

A. A noninvasive test to detect obstructive and/or restrictive lung

diseases; all results are based on standardized charts of predicted
values by percentage
1. Obstructive: COPD (emphysema and chronic bronchitis), asthma,
cystic fibrosis; also bronchiectasis or bronchiolitis in children 2.
Restrictive: may be related to lung pathology or extrinsic factors (i.e.,
outside the lungs): pneumonia, sarcoidosis, TB, tumors, pulmonary
edema, pulmonary fibrosis, scoliosis, obesity, ascites 3. Mixed or
neuromuscular: ALS, diaphragmatic paralysis, myasthenia gravis,
muscular dystrophy, polio
B. May be used to evaluate patients with SOB, dyspnea on exertion
(DOE), or chronic cough or as a preop assessment tool C. Do not test
the patient during an acute illness/exacerbation—wait for at least 6
weeks after the illness has resolved D. PFT interpretation (Table 6-2)
1. Forced vital capacity (FVC): total volume of air forcefully exhaled after
a full inspiration; used to determine the degree of severity of restrictive
diseases 2. FEV1: volume of air forcefully expired in the first second
during maximal expiratory effort; measures large airways and normal

196
 is >80% predicted 3. FEV1/FVC ratio: used to determine the overall
degree of severity of lung diseases; normal is ≥70% (obstructive lung
disease can be as low as 20% to 30%; restrictive disorders may be near
normal) 4. Total lung capacity (TLC): air volume in lungs after
maximum inspiration; used to determine difference between
obstructive and restrictive diseases
Table 6-1
Predicted Peak Expiratory Flow Rate

Child and Adolescent Female (Age 6-20 yrs)

Height (in): 42 46 50 54 57 60 64 68 72
Age: 134 164 193 223 245 268 297 327 357
6
8 153 182 212 242 264 287 316 346 376
10 171 201 231 261 283 305 335 365 395
12 190 220 250 280 302 324 354 384 414
14 209 239 269 298 321 342 373 403 432
16 228 258 288 317 340 362 392 421 451
18 247 277 306 336 358 381 411 440 470
20 266 295 325 355 377 400 429 459 489
Child and Adolescent Male (Age 6-20 yrs)
Height (in): 44 48 52 56 60 64 68 72 76
Age: 99 146 194 241 289 336 384 431 479
6
8 119 166 214 261 309 356 404 451 499
10 139 186 234 281 329 376 424 471 519
12 159 206 254 301 349 396 444 491 539
14 178 226 274 321 369 416 464 511 559
16 198 246 293 341 389 436 484 531 579
18 218 266 313 361 408 456 503 551 599
20 238 286 333 381 428 476 523 571 618
Adult Female (Age 25-80 yrs)
Height (in): 58 60 62 64 66 68 70 72 75
Age: 350 365 379 394 409 424 439 498 515
25
30 342 357 372 387 402 417 431 489 506
35 335 350 364 379 394 409 424 480 497
40 327 342 357 372 387 402 416 471 488
45 320 335 349 364 379 394 409 462 479
50 312 327 342 357 372 387 401 453 470
55 305 320 334 349 364 379 394 444 461
60 297 312 327 342 357 372 386 435 452
65 290 305 319 334 349 364 379 426 443
70 282 297 312 327 342 357 371 417 434

197
 75 275 290 304 319 334 349 364 408 425
80 267 282 297 312 327 342 356 399 416
Adult Male (Age 25-80 yrs)
Height (in): 63 65 67 69 71 73 75 77 80
Age: 492 520 549 578 606 635 664 692 701
25
30 481 510 538 567 596 624 653 682 689
35 471 499 528 557 585 614 643 671 677
40 460 489 517 546 575 603 632 661 665
45 450 478 507 536 564 593 622 650 652
50 439 468 496 525 554 582 611 640 640
55 429 457 486 515 543 572 601 629 628
60 418 447 475 504 533 561 590 619 615
65 408 436 465 494 522 551 580 608 603
70 397 426 454 483 512 540 569 598 591
75 387 415 444 473 501 530 559 587 578
80 376 405 433 462 491 519 548 577 566
How to calculate predicted expiratory peak flow:

• Have the patient blow into the peak flow meter 3 times, reset the meter prior to each attempt;
then calculate the average.
• Divide the patient’s peak flow by the predicted peak flow; answer equals the percentage of
expected normal peak flow rate.
• Example: the patient is a 10-year-old male and 52 inches tall. The expected normal peak flow
would be 234. The patient’s average peak flow today is 100; 100 ÷ 234 = 0.427 (43% of normal).
After nebulizer treatment with albuterol, the patient’s peak flow is 200; 200 ÷ 234 = 0.85 (85% of
normal). An improvement is noted.
• Can be used as a guide to the patient’s condition at the time of examination and after nebulizer
treatment has been given to determine if beta2 inhalers (SABA) would be beneficial as a
treatment to decrease bronchospasm.

Table 6-2
How to Read PFTs Quickly

Function Normal Obstructive Restrictive Mixed

FVC >79% of predicted Decreased Mild: 60%-79% Decreased
Moderate: 40%-59%
Severe: <40%
FEV1 >79% of predicted Decreased* Decreased Decreased
FEV1/FVC >70% Mild: 61%-69% Normal to increased Decreased
Moderate: 45%-60%
Severe: <45%
Very severe: <35%
TLC† 100% >120% of predicted‡ Mild: 65%-80% Decreased
Moderate: 50%-65%
Severe: <50%
*If decreased more than FVC, suggests emphysema.

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†Defining
factor for restrictive disease.
‡Due
to decreased recoil of lung tissue (e.g., COPD).

Asthma

I. Description

A. Chronic inflammatory condition of the airways; associated with

widespread bronchospasm and variable airflow obstruction that is
reversible either spontaneously or with treatment B. Symptoms can be
triggered by the following:
1. Environmental allergens (e.g., smoking, dust mites, pets) or
occupational conditions (e.g., chemical irritants, pollution) 2. Exercise
(timing of symptoms related to physical activity in healthy people:
exercise induced asthma [EIA]) 3. Drugs (e.g., aspirin, NSAIDs, beta-
blockers)
4. Structural defects (nasal polyps)
5. Exposure to cold temperature and foods (e.g., ice cream)
6. Emotional stressors (e.g., crying and laughing, which cause
bronchoconstriction) 7. Foods and drinks (e.g., peanuts, food
additives), GERD
II. Signs and symptoms

A. Mild-to-moderate attacks
1. Persistent cough (may be the only sign) occurring at night or with
exercise, especially in cold and dry air 2. Episodic, mild, diffuse
wheezing
3. Chest tightness
4. Dyspnea, tachypnea, SOB
5. Speaks in short sentences with minor difficulty
B. More severe attacks/poor control
1. Loud wheezing
2. Use of accessory muscles and intercostal retractions
3. Distant breath sounds, hyperresonance
4. Can only speak in short phrases

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 C. Ominous signs
1. Fatigue, drowsiness, or confusion
2. Diaphoresis; cyanosis, especially of lips
3. Inaudible breath sounds with diminished wheezing (“silent chest”)
4. Inability to lie flat
5. Can only speak in short phrases
III. Diagnostic testing for mild-to-moderate exacerbations

A. CBC may show an elevated WBC count, eosinophilia

B. PEF <60% predicted (see Table 6-1) C. CXR: hyperinflation
D. Pulse ox <90%
E. Complete PFT (e.g., flow rates, prebronchodilator and post
bronchodilator lung function, lung volumes, and diffusion) should be
done at least yearly (with trending) or after major medication changes
IV. Treatment (see Table 6-3 for Drugs for Asthma/COPD)

A. Mild intermittent: daytime attacks >2 times a week and nocturnal

symptoms <2 times a month; asymptomatic with normal PEF between
attacks; does not interfere with normal activity
1. Spirometry would be normal with FEV1 >80% predicted; obtain PFT
q2yr
2. Long-term control requires no daily medications, only rescue
medications 3. Patient education: reinforce at each visit; use an asthma
educator (if available)
a) assess patient’s correct use of inhalers initially and when changing
type b) allergen control (see Allergen Control Measures) c) consider
using daily peak flow monitoring to help with self-management
4. Rescue inhaler: short-acting beta2-agonist (SABA)
B. Mild persistent: >2 episodes a week but <1 time daily and nocturnal
symptoms >3 to 4 times a month; exacerbations may inhibit activity
1. Spirometry: PEF >80% predicted; FEV1/FVC normal; obtain PFT q2yr
or more often if there is an increase in exacerbations 2. Long-term
control

200
a) requires inhaled corticosteroid (ICS) daily
b) alternate therapy
(1) sustained-release theophylline; must monitor closely for therapeutic
levels or (2) leukotriene receptor antagonists
3. Patient education: as with mild intermittent
4. Rescue inhaler: SABA
5. Monitor the number of exacerbations; if SABA is used qd or with
increasing frequency, may need additional long-term therapy 6.
Consult the physician for ongoing therapy
C. Moderate persistent: daily daytime episodes and nocturnal symptoms
>1 time a week; affects activity and symptoms cause some limitation in
ADLs; daily use of SABA
1. Spirometry: FEV1 60% to 80% predicted with PEF >30%; obtain PFT q1-
2yr depending on exacerbations or medication changes 2. Long-term
control requires daily ICS
a) may use ICS with a long-acting beta2-agonist (LABA) for
bronchodilation b) sustained-release theophylline can be used along
with ICS for the relief of nocturnal symptoms c) may use a leukotriene
receptor antagonist
3. Patient education: as with mild intermittent
4. Quick relief: SABA as a rescue inhaler prn; if used daily, treatment
may need to be reevaluated 5. Consult the physician about referral
D. Severe persistent: frequent daytime and nocturnal episodes; continual
symptoms that limit ADLs and physical activity
1. Spirometry: FEV1 <60%; obtain PFT q1yr
2. Long-term control
a) daily medications include ICS and LABA
b) may require sustained-release theophylline and/or oral corticosteroids
in short-burst therapy or low-dose long-term therapy c) may use a
leukotriene receptor antagonist
3. Patient education: as with mild intermittent
4. Quick relief: SABA as a rescue inhaler prn; if used daily, treatment

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 may need to be reevaluated 5. Refer to a pulmonologist if the
symptoms cannot be controlled; emergent referral to ED if ominous
signs present
Table 6-3
Drugs for Asthma/COPD

Child Dose (Use of a Spacer

Drug Adult Dose
Will Improve Delivery)
Inhaled Short-Acting Beta2-Agonist (SABA) (Asthma or COPD Rescue or Maintenance)
Albuterol nebulized solution (5 2.5-5 mg q20 min × 3 doses, 0.15 mg/kg q20 min × 3 doses,
mg/ml) then 2.5-10 mg q4h prn then 0.15-0.3 mg/kg q4h prn
Albuterol MDI 90 mcg 2 puffs q4-6h 1-2 puffs q4-6h
Can be used 10-30 min before Can be used 10-30 min before
exercise exercise
Levalbuterol (Xopenex) 0.63-1.25 mg solution q6-8h 6-11 yrs: 0.31 mg nebulized
nebulized solution: 1.25 mg/3 Do not mix with other drugs solution tid
ml, 0.63 mg/3 ml, 0.31 mg/3 ml No dilution needed >11 yrs: 0.63 mg nebulized
solution tid
Do not mix with other drugs
No dilution needed
Anticholinergics (COPD Maintenance Only)
Ipratropium (Atrovent) 0.5 mg q30 min × 3 doses then Not recommended
solution for nebulizer: 0.5 q2-4h prn
mg/vial Can be mixed with beta2-
agonists
Not used as first-line therapy
Ipratropium (Atrovent) MDI 18 1 puff 3-4 times a day Not recommended
mcg
Long-Acting Muscarinic Antagonist* (LAMA) (COPD Maintenance Only)
Tiotropium (Spiriva) 1 puff daily Not recommended
Umeclidinium (Incruse Ellipta) 1 puff daily Not recommended
Aclidinium (Tudorza Pressair) 1 puff bid Not recommended
Long-Acting Muscarinic Antagonist/Long-Acting Beta2-Agonist* (LAMA/LABA) (COPD
Maintenance Only)
Umeclidinium/vilanterol 1 puff daily Not recommended
(Anoro Ellipta)
Inhaled Corticosteroid† (ICS) (Asthma and COPD Maintenance Only)
Beclomethasone dipropionate 40-80 mcg 1-4 puffs bid (if the 5-11 yrs: 40-80 mcg 1 puff bid
(QVAR) 40 and 80 mcg MDI patient is using Start 40 mcg/spray bid and
bronchodilators alone) increase the dose as needed
Budesonide (Pulmicort) DPI 2 puffs bid 1-2 puffs bid
(dry powder inhaler) 90-180
mcg
Budesonide (Pulmicort) 0.25 0.5 mg nebulized qd to bid 0.25 mg nebulized qd to bid
mg or 0.5 mg solution for
nebulizer

202
Fluticasone (Flovent HFA) 44, 2 puffs bid 4-11 yrs: 44 mcg, 1-2 puffs bid
110, 220 mcg ≥12 yrs: use adult dose

Fluticasone (Flovent Rotadisk) 1-2 puffs bid (start with 1 puff 4-11 yrs: 50-100 mcg bid
50, 100, 250 mcg and increase as needed) ≥12 yrs: use adult dose
Long-Acting Beta2-Agonist (LABA)
Formoterol* (Foradil aerolizer) 1 cap q12h >5 yrs: 1 cap q12h
12 mcg/cap DPI Use with an asthma controller Can use for EIA: 1 cap inhaled
Used for asthma and COPD medication approximately 15 min before
maintenance Can use for EIA: 1 cap inhaled activity
approximately 15 min before
activity
Salmeterol* (Serevent discus) 1 puff q12h >4 yrs: 1 puff q12h
50 mcg/blister DPI Can use for EIA: 1 puff Can use for EIA: 1 puff
Used for asthma and COPD approximately 30-60 min approximately 30-60 min
maintenance before activity before activity
Indacaterol* (Arcapta neohaler) 1 cap qd No dosing for pediatrics
75 mcg/cap DPI
Used for COPD maintenance
Arformoterol (Brovana) 15 2 ml bid No dosing for pediatrics
mcg/2 ml for nebulizer
Used for COPD maintenance
Combination of Long-Acting Beta2-Agonist* and Inhaled Corticosteroid† (LABA/ICS)
(Maintenance Only)
Fluticasone/salmeterol* 1 puff q12h 4-11 yrs: 100/50 mcg 1 puff
(Advair) 100/50, 250/50, or Start with 100/50 mcg bid if q12h
500/50 mcg DPI the patient is not taking any ≥12 yrs: use adult dosing
Used for asthma maintenance other steroid
If the patient is using steroids,
start with 250/50 mcg, up to
500/50 mcg bid
Mometasone/formoterol 2 puffs bid >12 yrs: 2 puffs bid; start with
(Dulera) spray MDI 100/5, the lowest dose
200/5 mcg
Used for asthma maintenance
Budesonide/formoterol 2 puffs bid >12 yrs: 2 puffs bid; start with
(Symbicort) spray MDI 80/4.5, the lowest dose
160/4.5 mcg
Used for asthma and COPD
maintenance
Fluticasone/vilanterol (Breo 1 puff q24h No pediatric dose
Ellipta)
Used for COPD maintenance
Others
Theophylline: in liquid, Starting dose 10 mg/kg/day, Elixophyllin 80 mg/15 ml
sustained-release tablets, and not to exceed 900 mg/day 1-9 yrs: 20-24 mg/kg/day
capsules Monitor liver enzymes 9-12 yrs: 16 mg/kg/day
Not recommended for COPD 12-16 yrs: 13 mg/kg/day

203
 Dosing is bid
Monitor liver enzymes
Systemic oral steroids: 5-60 mg qd 1-2 mg/kg daily
Prednisone tablets Usually given as “burst” Usually given as “burst”
Prednisolone: therapy; start with a high dose therapy; start with a high dose
Pediapred 5 mg/5 ml and taper over 10-14 days and taper over 10-14 days
Prelone 15 mg/5 ml
Leukotriene Modifiers (Asthma Maintenance Only)
Zafirlukast (Accolate): 10 mg or 20 mg bid 5-11 yrs: 10 mg bid
20 mg tablet Take on empty stomach >12 yrs: 20 mg bid
Take on empty stomach
Montelukast (Singulair) 4 or 5 10 mg hs 2-5 yrs: 4 mg hs
mg chew or 10 mg tablet 6-14 yrs: 5 mg hs
Zileuton (Zyflo) 600 mg tablet 600 mg qid with meals and hs >12 yrs: 600 mg qid; may take
Zileuton CR 600 mg ER 1200 mg bid; can take with with food
food >12 yrs: 600 mg bid with food
Phosphodiesterase-4 Inhibitor (Only COPD)
Roflumilast (Daliresp) 500 mcg qd Not recommended
*Contraindicated
with soy, milk, or or peanut allergy.
†Rinse
mouth after use.

P r a c t i c e Pe a r l s f o r A s t h m a

• Patient and family education regarding cause, triggers of symptoms, treatment, and control
of allergens/irritants is of utmost importance in controlling asthma. Treat any underlying
illness or refer to an allergist for testing.
• Early diagnosis and treatment are essential for maintaining normalcy.

• Minimize the severity of attacks with early treatment.

• Worsening nocturnal symptoms may indicate worsening of the disease.
• Medications
■ Inhaled corticosteroids DO NOT affect long-term growth in children.
■ Nebulized or inhaled albuterol is preferred over the liquid oral form
(which causes severe irritability).
■ If more than two SABA inhaler canisters are used a month, asthma
control is in question.
■ Use albuterol inhaler 15 minutes before activity to control the

204
 symptoms of exercise-induced asthma (EIA).
■ Patients should not trust the “float” test to determine fullness of the
inhalers (not accurate); most new inhalers have counters on the
canister.
■ Always use an aerochamber (spacer) with inhalers if possible. This
delivers about 30% more medication into the lungs. This is a separate
prescription.
• Instruct the patient to perform peak flow testing daily or weekly, depending on control, and
to monitor asthma symptoms according to peak flow “personal best” calculations. There
should be a plan in place to allow the patient to start therapy immediately when
exacerbations occur.
• GERD can worsen asthma symptoms.

Allergen control measures

Because environmental stimuli exacerbate asthma, allergen control is important. These measures
can be beneficial for any allergy-induced symptoms; they must be used daily at home and other
places where the person spends a lot of time.

I. Outdoor allergens

A. Determine if there is a particular aggravating season

B. Keep windows closed; use air-conditioning with ultrasensitive filters
C. When in a car, keep windows up and use air-conditioning
D. Limit outdoor activity to early morning or late evening; wear a mask
if doing yard work
II. Indoor allergens

A. Wear a mask when vacuuming or cleaning draperies

B. Limit the number of houseplants at home
C. Dust mite control includes the following:
1. Covering or encasing mattresses and pillows with plastic covers
2. Washing bedding weekly in hot water
3. Replacing bedroom carpets with hardwood floors or linoleum
4. Vacuuming house and bedroom carpets frequently using HEPA
ultrasensitive filters to remove pet dander and dust; consider having
ducts cleaned and changing air intake filters quarterly 5. Removing
any upholstered pieces of furniture and other dust collectors

205
 D. Decrease humidity in the house, especially in the bedroom
E. Limit exposure to cockroaches and their feces using the following
measures:
1. Promptly cleaning up after meals and sealing all food sources and
dishes tightly 2. Sealing gaps around the kitchen and bathroom pipes
3. Using either OTC roach bait stations or professional extermination
F. Cat and dog allergens are other possible causes
1. If possible, remove cats and/or dogs from the environment; if not
possible, keep pets out of the bedroom and off frequently used
furniture
2. Minimize contact with animals whenever possible
3. Wash pets weekly in water to decrease dander and loose hair and
check for fleas or ticks

Chronic obstructive pulmonary disease

I. Description: an obstructive airway disease that may be considered partially reversible or

irreversible. COPD includes both chronic bronchitis and emphysema, which are characterized by
remodeling and narrowing of small airways. There is no cure, only management of disease
processes with lifestyle changes.
II. Causative factors

A. Chronic exposures: tobacco smoke, air pollution, airway infections,

and dust and chemical exposure from environmental sources (e.g.,
irritants, fumes) B. Familial factors or hereditary factors (i.e., α-1-
antitrypsin glycoprotein) C. Allergy predisposition and
hyperresponsiveness
III. Signs and symptoms: usually present for >3 to 6 months in the last 2 years

A. Cough, usually chronic and worse in the mornings (usually the first
sign); may have rhonchi, hyperresonant breath sounds or wheezes B.
Chronic sputum production: excessive amount and is clear to white
C. Progressive, persistent dyspnea with any activity
D. Frequent viral or bacterial URIs
E. Feeling of anxiousness
F. Barrel chest appearance

206
 G. Central cyanosis and cachexia are later signs
H. Exacerbations are common and need to be treated quickly to prevent
complications and ED visits; see Action Plan under treatment
IV. Diagnostic tests

A. CXR: hyperinflation and air trapping with a flattened diaphragm,

bullae; decreased vascular marking and may have cardiomegaly B.
CBC may show elevated Hct
C. Obtain baseline pulse ox with an oxygen saturation goal of 88% to
90%; criteria for oxygen: pulse ox at rest <88% and increases to >88%
with O2 at 2 to 3 LPM
D. Peak flow shows obstructive pattern with <60% predicted values (use
this to monitor progression of the disease) E. If symptoms of COPD
occur at <40 years of age, consider testing for α-1-antitrypsin
deficiency F. Pulmonary function (see Table 6-2)
1. TLC increased
2. FVC decreased to normal
3. FEV decreased
4. FEV1/FVC decreased
V. Lifestyle changes to improve survival rates

A. Smoking cessation reduces the risk of progression

B. Encourage the patient to wear a mask when working with irritants,
fumes, or particulate matter C. Avoid temperature extremes; if not
possible, wear protective cover over the mouth and nose in the cold D.
Humidification at home, especially in winter
E. Bronchial hygiene with pursed lip breathing and deep breathing
before coughing F. Increase fluids if not contraindicated because of HF
G. Participate in a pulmonary rehab program as soon as diagnosed
H. Use of oxygen and daily medications
I. Encourage annual flu shot and the pneumonia immunizations
VI. Maintenance pharmacotherapy (for symptom control; does not affect long-term decline, see
Table 6-3)

A. Mild intermittent COPD with FEV1 >80% predicted and FEV1/FVC

207
 >70%
1. SABA prn for symptom control
2. Overnight pulse ox and, if indicated, consider nocturnal O2
B. Moderate COPD with FEV <80% predicted and FEV1/FVC <70%
1. Daily use of SABA and an anticholinergic inhaler 2 to 4 times qd,
depending on the symptoms 2. Consider ICS daily
3. Consider inhaled LABA bronchodilator/steroid combination and a
long-acting anticholinergic 4. Intermittent-to-continuous O2
C. Moderate-to-severe COPD with FEV <50% predicted and FEV1/FVC
<70%
1. Daily use of a LABA bronchodilator + corticosteroids
2. Long-acting inhaled anticholinergic
3. Continuous O2
D. Severe COPD with FEV <30% predicted and FEV1/FVC <70%: qd use
of the following:
1. Nebulized bronchodilator/ipratropium plus either inhaled or nebulized
corticosteroids or 2. LABA/ICS plus a long-acting anticholinergic
inhaler or LAMA
3. Continuous O2
VII. Treatment for exacerbations (see Action Plan in Table 6-4)

A. Establish a written action plan for treatment of exacerbations. In order

for the plan to work, the patient must understand how COPD occurs,
what exacerbations are like, and how to treat and must have the
medications at home to treat. These plans may not affect the overall
outcome but may decrease the frequency of exacerbations and hospital
visits.
B. Increase the frequency of inhaled SABA and/or add an inhaled
anticholinergic; if the symptoms are poorly controlled, switch to
nebulized medications C. Oral corticosteroids 40 mg daily for 5 days
D. Antibiotics for 10 days if the sputum is purulent or increased with
worsening dyspnea
1. Amoxicillin 500 mg tid

208
 2. Amoxicillin/clavulanate 500 to 875 mg bid
3. Doxycycline 100 mg bid
4. TMP/SMZ DS bid
5. Levafloxacin 250 to 500 mg qd
E. Continuous O2 until the symptoms improve
F. Guaifenesin daily may help cough and mucus clearance
G. Refer to ED if the condition is not improving or there is obvious
respiratory distress
Table 6-4
COPD Action Plan*

Symptoms Actions to Start

Mild Worsening of COPD
Mild increase 1. Increase inhaled albuterol†
in fatigue
and SOB 2. Rest and increase fluid intake
Mild increase 3. Increase O2 whenever resting
in cough and
4. No smoking and no exposure to smoke/allergens
sputum
production
Some
improvement
in symptoms
with daily
inhalers
Mild feeling
of anxiety
Early Onset of Exacerbation Symptoms
More 1. Stop daily inhalers (except steroids), start nebulized albuterol or levalbuterol
breathless
with ipratropium qid, and add 3 ml of saline to each dose for next 3 days; may
than usual use nebulized saline between doses if needed 2. If using O2 prn, increase to
with less
continuous use; may increase by 1 L/min (do not exceed 4 L/min) 3. Start
energy
prednisone 40-60 mg qd for 3-5 days and continue with inhaled steroids 4. If
↑ coughing
the sputum is thick and yellow, start (antibiotic) for 5-10 days 5. Rest
during the
frequently and use pursed lip breathing
day and
cough 6. No smoking or exposure to smoke
disturbs 7. Call office if the symptoms do not improve in 24 h
sleep more
8. If the symptoms improve, return to prior treatment but make an
than usual
appointment with PCP to review the plan
Using rescue
inhalers
more often

209
than usual
Rescue and
daily inhalers
do not affect
symptoms
Phlegm is
thicker and
more difficult
to cough up
Sputum
changing
colors
Feeling of
having a
“chest cold”
and poor
appetite
↑ swelling in
ankles in the
mornings
↑ anxiety
without
known cause
Late Onset of Exacerbation Symptoms
SOB at rest 1. Call 911 or go to ED
and with O2
2. While you are waiting for help to arrive: start nebulizer with albuterol or
Inability to
levalbuterol, add 3 ml saline to treatment, AND use nebulized steroids
carry out
daily activity
Unable to
sleep because
of ↑ cough/↑
SOB
Feeling of
confusion,
tiredness,
fatigue
Feeling of
“doom,”
agitation, ↑
anxiety
Fever and
chills
Chest pains
and/or
coughing up
thick yellow
sputum or

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 blood
*This
is a general plan and should be customized for each patient.
†Some
patients may feel more comfortable with inhalers and can continue with routine inhalers, but increase the number of rescue
inhalations during exacerbations only.

Table 6-5
Adult Outpatient Drug Therapy for Community Acquired Pneumonia*

Drug Class Dosage

Macrolides Azithromycin (Z-Pak) 500 mg on day 1; 250 mg on days 2-5
Clarithromycin (Biaxin) 250 mg q12h
Penicillins and beta-lactam Amoxicillin 500-1000 mg tid
inhibitors Amoxicillin/clavulanate (Augmentin) 875 mg bid
Tetracycline Doxycycline 100 mg bid
Cephalosporin (second or third Cefaclor (Ceclor) 500 mg tid
generation) Cefprozil (Cefzil) 250-500 mg bid
Cefuroxime (Ceftin) 250-500 mg bid
Cefpodoxime (Vantin) 200-400 mg bid
Ceftriaxone (Rocephin) 500-1000 mg IM qd
Fluoroquinolone (has Levofloxacin (Levaquin) 750 mg
antipseudomonal activity) Moxifloxacin (Avelox) 400 mg
Other antibiotics Linezolid (Zyvox) 400-600 mg po q12h for 10-14 days (covers
MRSA and other resistant bacteria)
*Antibiotics
are usually given for 10 days but may be needed longer, depending on the comorbidity/modifying factors. See Chapter 17 for
drug therapy for children with pneumonia.

Acute bronchitis

I. Description

A. Causative agents: rhinovirus, Bordetella pertussis, adenovirus,

influenza virus, and other infectious agents B. Occurs more frequently
in smokers and usually lasts longer; subsequent bacterial infections
may occur more frequently in smokers
II. Signs and symptoms

A. URI symptoms: nasal congestion, rhinitis, sore throat, malaise, and

low-grade fever B. Cough follows shortly after and may last up to 3
weeks
C. May or may not have wheezing and SOB
D. Sputum production, dyspnea
III. Treatment: symptomatic treatment; is usually a viral illness and antibiotics are not needed

A. Antitussives, expectorants, antihistamines, and decongestants

B. SABA bronchodilators (see Table 6-3), either inhaled or nebulized C.

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 NSAIDs or Tylenol for general discomfort

Community-acquired pneumonia (CAP)

I. Definition: acute pulmonary infection in a person not recently hospitalized; caused by

migration of bacteria from the upper airway to the lower airways

A. Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella

catarrhalis: cause high fever and productive cough B. Mycoplasma
pneumoniae, Legionella, and respiratory viruses: cause dry cough with
diffuse patchy lung findings on CXR
II. Signs and symptoms

A. Sudden onset and rapid progression of fever, rigors, cough with

purulent sputum production, and lobar consolidation on imaging (e.g.,
S. pneumoniae, H. influenzae) B. General symptoms of CAP
1. Tachypnea, tachycardia, cyanosis
2. Fever, malaise, myalgia
3. Exertional dyspnea, pleuritic chest pain
4. Anorexia, weight loss
5. Decreased breath sounds, wheezing, rhonchi, crackles
6. Egophony (“e” to “a” sound) on auscultation, pleural friction rub,
dullness to percussion 7. Sputum production
III. Diagnostic testing

A. Pulse ox results should be >95% on room air and should not drop with
exertion B. CBC and complete metabolic profile (i.e., if the patient is
>65 years of age, comorbidity exists, or possible hospital admission)
1. Leukocytosis with left shift may indicate bacterial infection; elderly
people may not have a competent immune system to generate this
response 2. Leukopenia (leukocytes <5000 mm3) may indicate
impending sepsis 3. Hgb <9 mg/dl and/or Hct <30% is indicative of
higher mortality
4. CXR (AP and lateral) should show frank consolidation in the area of
pneumonia and possible pleural effusion, but false-negative results can
occur with dehydration or very early onset of pneumonia
a) CXR is indicated in all symptomatic patients aged >40 years, current

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 smokers, or past smokers; repeat CXR should be obtained in 4 to 6
weeks no resolution or if still symptomatic, recommend referral to
pulmonologist b) if the patient has clinical signs and symptoms of
pneumonia but CXR does not show it, treat the patient for pneumonia
IV. Treatment: depends on the patient’s condition, suspected pathogen, and any
modifying/comorbidity factors for the patient (see Table 6-5, Adult Drug Therapy for
Pneumonia)

A. No comorbidity and has been healthy: use a macrolide or doxycycline

B. Person with comorbidity factors (see D below)
1. Heart, lung, renal, liver disease
2. DM, alcoholism, asplenia, malnutrition
3. Currently taking >10 mg prednisone daily
C. Person with modifying factors related to risk (see D below)
1. Age >65 years, alcoholism, or multiple medical comorbidities: at risk
for drug-resistant pneumococcal infection 2. Living in a long-term care
facility or with multiple medical comorbidities: at risk for infection
with an enteric gram-negative organism 3. Structural lung disease and
recent broad-spectrum antibiotic use for >7 days in the last month: at
risk for Pseudomonas infection 4. Current exposure to daycare
situations increases the risk for viral and streptococcal infections
D. If multiple comorbidity or modifying factors, may need a combination
of fluoroquinolone and macrolides, cephalosporin, or penicillin
antibiotics E. Consider O2 therapy for the duration of illness if pulse ox
drops <88% at rest or with activity F. Other pharmacologic therapies
1. NSAIDs or Tylenol for discomfort
2. Consider a nebulized bronchodilator and also an anticholinergic if a
smoker 3. Antitussives with nocturnal cough; consider benzonatate
(Tessalon Perles) for cough during the day and possible narcotic cough
suppressant at night 4. Consider stopping PPI (or switch to an H2
blocker) for 1 month after the illness subsides, if possible, because of
the increased risk of recurrent pneumonia
G. Nonpharmacological
1. Maintain adequate hydration, humidifier at home, rest
2. Follow-up in the office in 24 to 48 hours and if not improving, refer to

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 ED
H. After the illness has resolved, consider annual flu vaccine and
pneumococcal vaccines (if applicable)

Tuberculosis (TB)

I. Description

A. Primary lung infection acquired via droplets from contaminated

people. Usually the TB bacterium is inhaled, the normal defense
system is activated, and the bacterium is walled off without further
incident; 90% to 95% of TB bacteria are dormant.
B. TB can become active when the patient’s defenses undergo periods of
stress or are fighting off current infections, with corticosteroid therapy,
or with aging of the immune system C. Common sites are apices of the
lungs, but disseminated TB can affect any body system D. The risk of
TB increases with chronic disease, drug abuse, and living in a nursing
home or a crowded home with poor hygienic conditions
II. Signs and symptoms

A. Fatigue; unintentional weight loss, anorexia

B. Fever (usually low grade)
C. Night sweats lasting longer than 1 to 3 weeks
D. Productive cough (initially dry, progresses to purulent; may see
blood) E. Latent TB usually is asymptomatic and is diagnosed with a
TB skin test
III. Diagnostic testing

A. Tuberculosis skin test (TST) is a screening test only; interpret in 48 to

72 hours and measure induration, not redness. Obtain CXR with any
positive TST.
1. Induration ≥5 mm is positive in a patient with any of the following:
a) HIV
b) close contact with someone with TB
c) immunosuppression
2. Induration ≥10 mm is positive: if the patient

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 a) is a recent immigrant from a high-prevalence country
b) is an IV drug user
c) is a resident or employee of a high-risk facility (e.g., nursing home,
correctional facility, hospital, homeless shelter, or works in laboratory
setting) d) has a comorbid illness (e.g., DM, chronic renal or liver
disease, malnourished) or is aged <4 years exposed to adults at high
risk
3. Induration ≥15 mm is positive
4. People who have been vaccinated with BCG will have false-positive
TST but can still get TB; follow-up for any positive results
B. CXR
C. Sputum culture for acid-fast bacilli is time consuming and difficult to
obtain in clinical setting
IV. Treatment: identification and referral to the health department

Obstructive sleep apnea (OSA)

I. Description

A. Chronic airway obstruction while sleeping, which disrupts normal

sleep patterns B. Decreases O2 to vital organs
C. Can be a contributing factor for HTN, obesity, depression, and RLS
II. Risk factors

A. Obesity (e.g., BMI >30 kg/m2) is the primary factor

B. Large neck circumference and/or waist circumference
C. Traumatic craniofacial injuries and tonsillar hypertrophy
D. Male gender, age >40 years, and smoking
E. Type 2 DM, COPD
III. Signs and symptoms

A. Snoring and apnea periods and nocturnal restlessness are commonly

noted by sleeping partner B. Daytime sleepiness; napping/dosing off
during the day at inappropriate times C. Poor concentration, cognitive
deficits, and inattentiveness at work, school, or home D. Does not feel
rested upon awaking and frequently has morning headaches E. Poor

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 control of weight, HTN, and depression with mood swings
F. Sudden onset of a sleep episode, which may occur during activity (e.g.,
talking, driving, eating)
IV. Diagnostic testing

A. Overnight pulse ox
B. Epworth sleepiness scale (has not been validated but is used
frequently); considered normal if the score is ≤10/24
C. Polysomnography (gold standard for diagnosis) performed in a sleep
lab; test is positive if the apnea-hypopnea index (AHI: number of
apnea and hypopnea events/h) is >5 events/h with symptoms
1. Mild OSA: 5 to 14 events/h
2. Moderate OSA: 15 to 29 events/h
3. Severe OSA: >30 events/h
D. CBC, CMP, TSH (may be obtained to rule out other causes for
symptoms)
V. Treatment: referral to a pulmonologist or ENT depending on the cause VI. Follow-up

A. For changes in sleep habits and feeling of refreshed sleep

B. Monitor use of equipment; if the patient is not using his/her CPAP, ask
why and have them contact the supplier for alternative equipment C.
Monitor weight and BP

P r a c t i c e Pe a r l s f o r R e s p i r a t o r y C o n d i t i o n s

• Cough

• Anyone with persistent cough interfering with activity after treatment

for any illness should have a CXR (or repeat CXR) to rule out other
processes (e.g., cancer) and a complete PFT.
• When coughing is paroxysmal followed by intake of air at the end of a
series of coughs that sound like “whoop” and then the coughing “fit”
starts again:

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■ Consider pertussis and perform testing, especially in adults aged >45
years or in unvaccinated infants or children.
■ Pertussis usually responds well to a macrolide antibiotic.
■ Encourage Tdap vaccine once for all adults, especially those caring for
neonates/infants aged <6 months.
• For persistent cough or hoarseness without other signs or symptoms
related to an identifiable cause, consider silent reflux and try 1 month
of PPI or an H2 blocker or consider drug related (e.g., ACE cough).
• Differential causes of persistent or chronic cough: asthma, allergic
bronchitis, chronic bronchitis (usually from smoking), chronic
rhinosinusitis, OSA • Red flags for further evaluation: large amounts of
sputum daily (bronchiectasis); weight loss, fever and hemoptysis (TB,
cancer, lymphoma); dyspnea with cough (COPD, HF, fibrotic lung
disease) • Common antitussives for cough for short term relief:
dextromethorphan, OTC guaifenesin 1200 mg bid, benzonatate,
codeine
• When using nebulized albuterol or levalbuterol (Xopenex), consider adding 2 to 3 ml of
saline to each treatment; this will improve sputum production.
• Anyone with new-onset SOB should have a CXR (to rule out cancer or pulmonary fibrosis)
and a complete PFT.
• If OSA is suspected and the patient refuses polysomnography, consider overnight pulse
oximetry, which will determine if there is any nocturnal hypoxia. If the test is positive, order
nocturnal O2. This may improve the person’s quality of life and alertness during the day.
• With the new Durable Medical Equipment rules, ordering continuous O2 can be difficult. If
you suspect that the patient needs O2, perform the following:

• Check pulse ox at rest on room air and then ask the patient to walk 50
to 100 feet as fast as possible.
• Recheck pulse ox and if one or both of these tests are <88% on room air,
start oxygen at 2 to 3 LPM
• Recheck pulse ox while on O2 after 5 minutes at rest and after walking
50 to 100 feet as fast as possible; if pulse ox is >88% with O2, the patient
qualifies for home O2.

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CHAPTER 7

218
Eye, ear, nose, and throat conditions
For details regarding complete history and physical examination, see Chapter 1.

219
Ocular complaints

P r a c t i c e Pe a r l s f o r E ye s

• Eye examination

• Examining eyes can be simple or complicated, depending on what is

done.
• Record visual acuity in the right eye, left eye, and both eyes whenever
possible and ask the patient if his/her vision has been affected (see
Physical Examination, IV, C in Chapter 1).
• Determine the amount of inflammation: look at the eyes; where is the
redness in relation to the pupil? Is it localized or diffuse? Is it
symmetrical or asymmetrical in one or both eyes? Are the eyelids
swollen?
• Check pupils’ responses for equality and reactivity to light and
accommodation (PERRLA) and assess peripheral vision; failure of the
pupils to react appropriately or loss of peripheral vision indicates a
more serious problem.
• Fluorescein staining is used to detect injuries to the surface of the
cornea (e.g., abrasion, foreign body). This is done easily with minimal
discomfort and is a good tool for determining further care
requirements or referral urgency.
■ Make sure that the patient is not wearing contact lenses.
■ Instill local anesthetic eye drops. Do not let the patient touch his/her eyes
for the next 60 minutes: this can injure the cornea because the corneal
reflex is absent. If anesthetic drops give immediate relief, the problem
is on the surface; if pain remains, the pain is deep in the eye itself
(more serious).
■ Put a drop of saline on a fluorescein paper and touch the paper to the
inner lower eyelid. The conjunctiva will turn orange immediately (if it
does not, remoisten the fluorescein paper). Have the patient open and

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 close the eyelids a few times.
■ Using a cobalt blue pen light, inspect the cornea and under the eyelids;
if there is an injury or foreign object (FO), the dye will “stick” to the
area and is easily seen. Possible findings:
• “ice rink sign”: scratches on the cornea from blinking due to FO in the
upper eyelid • dendrite appearance: possibly herpes zoster or other
virus
• abrasions seen at the 3 and 9 o’clock positions on the cornea are
common with contact lens wearers • isolated dots across the cornea
from poorly fitted contact lenses or dry eyes • a lesion located in the
central vision (over the pupil) will decrease visual acuity and depth
perception
■ After the examination, irrigate the eyes with saline solution until clear.
Reevaluate in the same manner; an injury or FO is easily seen.
■ If abrasion is noted, instill antibiotic eye drops; tell the patient not to
touch his/her eyes for at least 1 hour if anesthetic eye drops were used
for examination.
■ Explain to the patient that orange drainage when blowing the nose is
from the dye running from the tear ducts to the nose.
■ Anesthetic eye drops are for examination purposes only and not for
pain relief.
• Eversion of the upper eyelid is an important tool for inspecting under
the upper lids for injury, FO, or swelling.
■ Remove contact lenses if in place; place a drop of local anesthetic into the
eye.
■ Ask the patient to look down and continue looking down through the
examination.
■ Firmly hold the eyelashes with the index finger and thumb of one hand
and place a cotton applicator tip at the base of the tarsus (top of the lid)
with the other hand.
■ Pull the lid down and toward you while you lift the lid directly up over
the applicator.
■ Hold the lid in place by holding the eyelashes and now examine the

221
 underside of the lid.
■ If FO is seen, use another cotton tip to gently remove.
• When instilling eye drops, place drop(s) into the inner canthus while the eye is closed and
then have the patient open the eyes; drop(s) will “run” into the eye. This is an easy,
“nonscary” way for children to receive eye drops.
• Recommended preventative eye examinations

• Children at risk: annually

■ Premature or low birth weight with known O2 supplementation ■
Strabismus, nystagmus
■ Known developmental delay, CP, hydrocephalus, seizures, etc.
• Children without risk
■ Birth to 24 months of age: at 6 months of age or as recommended ■ 2 to
5 years of age: about 3 years of age
■ 6 to 18 years of age: every 2 years if indicated
• Adults without risk or symptoms:
■ 18 to 60 years of age: about q3 to 5 years
■ >60 years of age: q1 to 2 years
• Adults at high risk: annually
■ DM with/without known retinopathy (examinations may be more
frequent with disease) ■ Any patient receiving chronic steroids,
chemotherapy, or biologic agent treatment ■ Patients with vision
issues involving cataracts or after cataract or other eye surgeries ■ Use
of any medications with ocular side effects (e.g., quetiapine) ■ Working
in occupations that are visually hazardous
• Vision complaints

• Sudden, painless, total loss of vision in one eye (possible acute central
retinal artery occlusion):
■ The retina is pale and edematous with a central macular cherry-red
spot.
■ Have the patient breathe into a paper bag (CO2 retention causes
vasodilatation) and immediately refer to ED or ophthalmologist.
• Deep, intense pain

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■ Corneal abrasion
■ Scleritis or iritis
■ Acute angle-closure glaucoma
■ Sinusitis from pressure behind the eye
■ Glaucoma
• Photophobia
■ Corneal abrasion
■ Iritis
■ Acute angle-closure glaucoma
• Halo vision
■ Corneal edema, including from contact lens overuse
■ Acute angle-closure glaucoma
• Blurred vision: consider abnormal tear production or acute angle-
closure glaucoma
• Pinguecula

• Small yellowish growth near the corneal edge, usually on the nasal side
• Usually from sun exposure/damage or chronic dry eyes
• Treat with NSAID drops (ketorolac ophthalmic [Acular] 1 gtt qid for 5
days) and artificial tears as needed.
• Pterygium

• Clear to flesh-colored, thin tissue growth (usually starts as pinguecula)

that can extend over the cornea and impair vision; commonly seen at
the 3 and 9 o’clock positions.
• Can cause irritation (sensation of “something in eye”) if swollen or
inflamed.
• Treat with natural tears frequently; when inflamed, can use NSAID
drops (i.e., ketorolac ophthalmic [Acular] 1 gtt qid for 5 days).
• Ophthalmology referral: urgent with acute-onset eye pain, diminished visual acuity, and
photophobia; nonurgent with chronic red eyes.

Common eye conditions

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I. Bacterial conjunctivitis

A. Signs and symptoms (unilateral or bilateral)

1. Itching and tearing
2. Yellow-green mucopurulent discharge from the inner canthus (usually
lasts all day) with conjunctival hyperemia (the limbus is spared) and
red, shiny appearance of the lower lids. With acute purulent discharge,
ask about sexual partners, as this could be a gonococcal infection and
can progress to vision loss.
3. No pain or vision disturbance, but may have blurred vision due to
tearing 4. The cornea is clear with mild eyelid swelling
5. No preauricular adenopathy (unless gonococcal infection)
B. Treatment
1. Antibiotic eye drops for 5 to 7 days; treat both eyes even if only one is
infected (to prevent spread to the other eye)
a) sodium sulfacetamide 10% (Bleph-10) 1 to 2 gtts tid
b) gentamicin 3% 1 to 2 gtts qid
c) ciprofloxacin 3.5% (Ciloxan) 1 to 2 gtts q2h while awake for 2 days,
then q4h (especially for contact lens wearers) d) azithromycin
(AzaSite) 1 gtt bid for 2 days, then 1 gtt qd
2. General measures
a) cold compresses on the eyes
b) artificial tears frequently
c) warn the patient and/or parents of the contagiousness of the disease
(1) a child cannot attend school/daycare until after using antibiotics for
24 hours (2) use separate towels, frequently wash hands, avoid hand
shaking
C. Refer to an ophthalmologist if not markedly better in 4 days or if
considering herpetic infection
II. Viral conjunctivitis

A. Signs and symptoms (unilateral followed by bilateral infection)

1. Burning, itching, tearing (may cause some blurred vision), and
conjunctival injection (limbus usually not spared) 2. Watery, mucoid

224
 discharge with mucous matting on lashes
3. Preauricular lymph node
4. Recent history of URI
B. Treatment
1. Cold compresses on the eyes
2. Gently cleanse with water (wipe from inside to outside of the eyes) 3.
Artificial tears to decrease irritation
4. Warn the patient of the contagiousness of the disease; recommend
frequent hand washing, use separate towels, avoid hand shaking 5. No
vasoconstrictors or antihistamine eye drops (may cause rebound
symptoms) 6. Consider antibiotic drops to prevent superinfection
C. Make a note in the chart to allow the child to return to school in 24
hours after starting treatment
III. Allergic conjunctivitis

A. Signs and symptoms (bilateral; if unilateral, investigate further)

1. Itching, redness, and watery discharge
2. Varying levels of conjunctival edema (chemosis), eyelid edema, and
redness 3. May have sneezing, rhinorrhea, “throat itching”
4. May have a history of atopic dermatitis
B. Treatment
1. Avoid allergens
2. Cold compresses; artificial tears to decrease irritation
3. Ketotifen (Zatidor) OTC: 1 gtt q8-12h prn
4. Prescription eye drops to relieve symptoms; avoid OTC allergy drops
containing tetrahydrozoline, which may cause rebound congestion
a) nedocromil 2% sol (Alocril) 1 to 2 gtts bid
b) olopatadine 0.1% sol (Patanol) 1 to 2 gtts bid
c) epinastine 0.05% sol (Elestat) 1 gtt qd
d) azelastine (Optivar) 1 gtt bid
e) ketorolac 0.5% sol (Acular) 1 gtt qid

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IV. Iritis

A. Signs and symptoms (unilateral)

1. Redness surrounding the cornea, called “ciliary flush” (i.e., appearance
of a red ring around the iris); no discharge 2. Pain and photophobia
caused by movement and light but no sensation of FO
3. The pupil is constricted
4. Caused by trauma, recent ocular surgery, arthritic psoriasis, and
herpes infections
B. Treatment: urgent ophthalmology referral
V. Corneal abrasion

A. Signs and symptoms (usually unilateral)

1. Pain and foreign body sensation
2. Photophobia and tearing with conjunctival hyperemia
3. Vision may be normal or decreased
4. Usual history of eye trauma or scratching or is a contact lens wearer
B. Diagnostic testing: stain with fluorescein (see Practice Pearls in this
chapter) and use cobalt blue light to inspect the eye for FO or abrasions
C. Treatment
1. Topical antibiotics for 5 to 7 days, especially if the patient is a contact
lens wearer
a) sodium sulfacetamide (Bleph-10) 1 to 3 gtts tid
b) ofloxin (Ocuflox) 1 to 2 gtts q2-4h for days 1 and 2; then qid for days 3
through 7
c) erythromycin ointment 1 cm ribbon up to 6 times a day
2. Antiinflammatory (e.g., Ketorolac [Acular] 1 gtt qid for 5 days) 3.
Observe qd until resolved; but if no improvement in 24 hours, send to an
ophthalmologist emergently
VI. Corneal ulcer (ulcerative keratitis)

A. Signs and symptoms (unilateral)

1. Foreign body sensation with conjunctival injection (limbus not spared)
2. Blurred and decreased vision with photophobia; may have corneal

226
 opacification 3. Severe pain with increased tearing, purulent discharge,
and hypopyon (pus in the anterior chamber)
B. Treatment: emergent referral to ED or ophthalmologist
VII. Acute angle-closure glaucoma

A. Signs and symptoms are caused by increased intraocular pressure

(unilateral or bilateral)
1. Acute-onset intense ocular pain, frontal H/A, N/V
2. Halos around lights, blurred vision, and fixed midposition pupils 3.
May be precipitated by dim light or certain drugs
B. Treatment: emergent referral to ED or ophthalmologist
VIII. Subconjunctival hemorrhage

A. Signs and symptoms (unilateral)

1. Blood located between the conjunctiva and sclera; may have felt a
stinging sensation at the time of hemorrhage 2. No change in visual
acuity
B. Caused by trauma, excessive straining (e.g., vomiting or coughing),
HTN, allergic symptoms C. Treatment
1. Rule out HTN
2. No treatment needed for eyes; reassure the patient that the redness
will resolve in ∼2 weeks 3. Can use artificial tears for mild irritation
4. Limit the use of aspirin and NSAIDs until complete resolution of
symptoms
D. Refer if the hemorrhage does not resolve or recurs within 2 weeks
IX. Hyphema

A. Signs and symptoms (unilateral)

1. Hemorrhage into the anterior chamber, which may be seen without an
ophthalmoscope; describe the amount of bleeding as a percentage of
the anterior chamber affected
2. Pain and blurred vision with some decrease in visual acuity
3. May or may not have photophobia
4. Increased intraocular pressure from blockage

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 B. Treatment: urgent referral to ED; have the patient sit in the semi-
Fowler’s position to decrease intraocular pressure; if obvious trauma,
shield the eye
X. Keratoconjunctivitis (dry eye)

A. Signs and symptoms (usually bilateral)

1. Irritation with redness and dryness
2. Burning and foreign body sensation or gritty feeling and blurred
vision
B. Caused by
1. Allergens (e.g., smoke, dust, fans)
2. Wearing contact lenses, eyelid disorders
3. Medications (e.g., antihistamines, diuretics, antiparkinsonian drugs,
anticholinergics, some antiarrhythmics) 4. Vitamin A deficiency
C. Treatment
1. Artificial tears in daytime (preservative-and decongestant-free) and
lubricating gel at night (gel causes less blurring of vision than
ointment) 2. Humidifier when sleeping
3. Elimination of causes
4. Flaxseed oil 1-2 g and/or omega-3 fatty acids 2 caps qd for 6 months 5.
Cyclosporine (Restasis) 1 gtt affected eye(s) q12h
D. Referral to an ophthalmologist if the condition persists
XI. Blepharitis

A. Signs and symptoms (usually bilateral)

1. Conjunctival redness and irritation with dryness and burning of the lid
margin 2. Dandrufflike debris on lid margins and eyelashes
3. No visual acuity defects or photophobia
4. Associated with rosacea and seborrheic dermatitis (see Chapter 5)
B. Treatment
1. Warm compresses on the eyelids and then removal of the debris via
gentle scrubbing with baby shampoo 2. Consider topical antibiotics for
7 to 10 days

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 a) bacitracin ointment thin ribbon on the eyelid border q6-8h after
cleaning b) sulfacetamide/0.2% prednisone (Blephamide) thin ribbon
(½ inch) tid and qhs
XII. Dacryocystitis

A. Signs and symptoms (usually unilateral)

1. Red, swollen, painful medial canthus around the tear duct opening;
purulent drainage from the lacrimal duct 2. Increased tearing with
mild-to-moderate pain; possible fever
3. The conjunctiva may be normal in appearance
4. May have an erythematous mass between the lower eyelid and nose 5.
May lead to orbital cellulitis
B. Causes: obstruction of the lacrimal sac due to infection from normal
skin flora, trauma, congenital obstruction, or nasal or sinus surgery
C. Treatment
1. Referral to ED emergently if acute cellulitis is present
2. If no cellulitis, may treat in office; obtain cultures of the discharge 3.
Antibiotic eye drops for 10 days in conjunction with oral antibiotics
a) sodium sulfacetamide (Bleph-10) 1 to 2 gtt tid
b) erythromycin (Ilotycin) 1 to 2 gtt qid
c) ofloxacin (Ocuflox) 1 to 2 gtt q1-6h for 7 to 10 days
4. Oral antibiotics bid for 10 days
a) doxycycline 100 mg
b) amoxicillin/clavulanate 500 mg
c) cephalexin 500 mg
d) ciprofloxacin 250 to 500 mg
5. Massage the ductal area and use warm, moist compresses
6. Follow closely q24-48h
XIII. Hordeolum (stye)

A. Signs and symptoms (unilateral)

1. Acute onset of reddened, painful, and localized swelling with an

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 abscess present 2. Usually self-limited and resolves in ∼5 to 7 days
B. Treatment
1. Warm, moist compresses multiple times daily
2. Antibiotic ointment may be required for 2 to 3 weeks
a) bacitracin ¼ to ½ inch q4h; when the infection is under control,
decrease the dosing frequency b) tobramycin ½ inch 2 to 3 times qd
c) erythromycin ½ inch 6 times qd
C. Refer to an ophthalmologist if the symptoms worsen, preauricular
lymphadenopathy occurs, or the hordeolum does not resolve after
treatment
XIV. Chalazion

A. Signs and symptoms (unilateral)

1. Gradual onset of sterile, localized, firm nodular tissue on the eyelid;
can last for months 2. Usually not painful but is irritating, especially
with eye movement 3. Usually does not affect vision
B. Treatment
1. Frequent warm, moist compresses
2. Local massage over the area 4 to 5 times qd after warm, moist
compresses 3. Treatment for suspected infection same as for blepharitis
if present (see Common Eye Conditions in this chapter)
C. Refer to an ophthalmologist if the symptoms persist

Common ENT conditions

I. Tinnitus

A. Description: sound heard by the patient that is not attributable to an

external sound (e.g., hissing, ringing, whining, buzzing)
1. May be unilateral or bilateral, consistent or intermittent
2. Usually perceived as louder at night (because there are fewer
distractions and extraneous sounds)
B. Possible causes
1. Aging and high noise levels for long periods of time

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 2. Cerumen impaction, acute and chronic OM, eustachian tube
dysfunction 3. Head and neck injuries, acoustic neuroma, DM, thyroid
disorders, and Meniere’s disease 4. Allergies
5. Medications
a) ASA, NSAIDs, loop diuretics, and caffeine
b) some antihypertensives (e.g., beta-blockers, especially metoprolol)
C. Diagnostic testing
1. Otoscopy with a pneumatic otoscope and insufflation
2. Rinne and Weber’s tests (see Figure 1-2) 3. Cranial nerve testing (see
Table 1-4) 4. CBC, ESR, ANA titer, Lyme disease titer (if suspected),
rheumatic factor, RPR (if syphilis is suspected), TSH, FBG
5. Audiology testing
D. Treatment
1. Hearing aids (if hearing loss is the cause) or tinnitus maskers (resemble
hearing aids but produce soft background noises) 2. Cognitive
behavioral therapy (e.g., relaxation techniques, biofeedback) 3.
Decrease salt intake
4. Medications that might help but not proven
a) ginkgo biloba (may improve circulation)
b) antianxiety drugs to help manage stress
c) melatonin (if having insomnia because of the noise)
II. Otitis Externa (OE)(also see Chapter 17)

A. Causes: bacterial or fungal agents, too much moisture in or aggressive

cleaning of the EAC
B. Signs and symptoms
1. Otalgia (worse with movement of pinna and tragus) and otorrhea
2. The EAC may be swollen, red, and painful with an exudate present.
a) acute bacterial: white thick mucus
b) chronic bacterial: bloody with granulation tissue
c) fungal: may be different colors (e.g., black, green, yellow)

231
 3. The TM can be normal or red; frequent complaint of fullness and loss
of hearing 4. With repeated infection, consider seborrhea, eczema, and
undiagnosed DM
C. Treatment
1. If possible, the provider can clean the EAC gently with a dry Q-tip or
try placing an ear wick to “soak up” the debris; do not attempt to curette
out the debris or to flush unless you can fully visualize the TM
2. After the EAC has been cleaned, use topical agents for 7 to 10 days;
may use ophthalmic drops, which are less expensive than otic drops
a) ciprofloxacin/dexamethasone (Ciprodex) otic 4 gtts bid (bacterial or
fungal) b) ofloxacin otic 5 gtts qd (bacterial or fungal; can be used with
TM perforation)
c) neomycin/polymixin B/hydrocortisone otic suspension 3 gtts 3 to 4
times a day (bacterial); do not use if suspected TM rupture d) 2% acetic
acid otic sol (VoSol) or 1%/2% hydrocortisone/acetic acid otic sol
(VoSol HC) (suspected fungal) 4 gtts q8h
3. Pain management with acetaminophen or ibuprofen
4. Discourage use of auralgan drops if ruptured TM suspected
5. Monitor diabetics or immunocompromised patients closely for
worsening disease 6. For 2 weeks, gently place cotton balls
impregnated with petroleum jelly into the EAC to keep water out
D. Prevention
1. Keep the ears dry; the patient should not use anything to clean or
scratch in the ears 2. After water exposure, use a blow dryer on low
setting to dry the EAC
3. To alleviate itching and prevent OE after swimming: instill a few drops
of vinegar, rubbing alcohol, or peroxide in the ears and immediately
let it drain out
III. Acute otitis media (AOM) (also see Chapter 17)

A. Cause can be either bacterial or viral

B. Signs and symptoms have acute onset
1. Otalgia, irritability, fever
2. TM

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 a) cloudy, bulging and impaired mobility
b) bright red or hemorrhagic appearance
c) may have bullae or perforations with or without purulent fluid
3. Loss of appetite, N/V
4. Tinnitus, vertigo, and hearing loss or ear stuffiness
5. H/A, irritability
C. Treatment
1. Pain management
a) oral: acetaminophen or ibuprofen; may need stronger pain meds
b) topical, if no perforation of the TM: antipyrine/benzocaine (Auralgan)
2. Antibiotics for 7 to 10 days
a) amoxicillin 500 mg tid
b) amoxicillin/clavulanate 500 mg tid or 875 mg bid
c) cefuroxime: 250 mg q12h
d) cefdinir 300 mg q12h
e) trimethoprim/sulfamethoxazole-DS 1 tab q12h
f) zithromycin: 500 mg for day 1 and then 250 mg days 2 to 5
D. Referral to ENT if the symptoms do not improve
IV. Otitis media with effusion (OME) (also see Chapter 17)

A. Causes: high-altitude activity, URI, allergies, or eustachian tube

dysfunction B. Signs and symptoms do not have acute onset
1. Decreased hearing
2. Feeling of fullness or pressure in the ear(s)
3. “Popping” sensation with yawning, swallowing, or nose blowing
4. TM retracted with clear to yellowish or bluish colored fluid; decreased
mobility and poor visibility of landmarks
C. Treatment
1. With mild symptoms, the condition often spontaneously resolves in 2
to 3 weeks but can take up to 12 weeks 2. Medications to consider

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 a) pseudoephedrine 30 mg tid
b) oxymetazoline (Afrin) 1 to 2 sprays q12h (NOTE: this should be used
only for 3 to 5 days because of nasal rebound congestion) c) loratidine
10 mg or cetirizine 10 mg or fexofenadine 180 mg qd
d) azelastine (Astelin) nasal spray 2 sprays each nostril bid
e) azelastine/fluticasone propionate (Dymista) 1 spray each nostril bid f)
consider nasal steroids (e.g., fluticasone, mometasone) 1 to 2 sprays
each nostril qd
3. Consider chewing gum or frequent autoinsufflation (trying to gently
“pop ears”, pinch nose closed and swallow or blow out with lips
closed, or blow up balloons) 4. Use hypertonic saline nasal spray often
(e.g., 8 to 10 times a day) or Neti Pot 2 to 3 times a day 5. Follow-up in
3 weeks and consider hearing testing
D. Referral to ENT or allergist if needed
V. Epistaxis

A. Causes include allergic rhinitis, dry outdoor conditions, infections,

use of OTC nasal sprays, trauma, foreign bodies, hereditary bleeding
disorders, leukemia B. Signs and symptoms
1. Usually no systemic symptoms; may have HTN or may be using
anticoagulants 2. May have petechiae or bruising
3. Bleeding may come from the nares (anterior) or go down the throat
(posterior); use a nasal speculum to visualize the nares and septum for
the site(s) of bleeding 4. May have blood in emesis
C. Treatment
1. Have the patient sit in an upright position and gently blow the nose to
remove clots 2. Hold the pressure by pinching the nares closed for 10
to 15 minutes by the clock
D. If bleeding is not controlled or if the patient’s status is questionable,
refer to ED; otherwise refer to ENT if there is recurrent bleeding
without an obvious cause E. Prevention
1. Use a humidifier in the bedroom and when traveling, if possible 2. Use
a small amount of water-based lubricant in the anterior nares at night
and during the day if the environment is dry 3. Use saline nasal spray
gently, frequently during the day and at hs 4. Review how to stop nose

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 bleeding with the pressure technique
5. Discourage digital manipulation, nose blowing, and excessive
sneezing (sneeze gently with mouth open) 6. Limit or discourage use
of NSAIDs or ASA, especially if the condition is chronic
VI. Allergic rhinitis

A. Signs and symptoms

1. Pruritus of the nose, eyes, palate, and oropharynx
2. Excessive tearing, allergic shiners, puffiness around eyes and
conjunctival injection 3. Cough and nasal congestion with sneezing,
rhinorrhea, and anosmia
B. Treatment
1. Limit exposure to allergens (see Allergen Control Measures in Chapter
6) 2. Steroid nasal spray 2 sprays each nostril
a) beclomethasone dipropionate (Beconase) bid
b) ciclesonide (Omnaris) qd
c) fluticasone propionate (Flonase) qd
d) mometasone (Nasonex) qd
3. Antihistamine (OTC) loratidine 10 mg, cetirizine 10 mg, or
fexofenadine 180 mg qd 4. Antihistamines (prescription)
a) desloratadine (Clarinex) 5 mg qd
b) levocetirizine (Xyzal) 2.5 to 5 mg q pm
5. Antihistamine nasal sprays each nostril bid
a) azelastine (Astelin) nasal spray 2 sprays
b) azelastine/fluticasone propionate (Dymista) 1 spray
6. Montelukast (Singulair) 10 mg hs (also used in people with asthma)
VII. Rhinosinusitis (also see Chapter 17)

A. Consider if symptoms are present for >10 days or the symptoms recur
after an initial period of improvement B. Signs and symptoms
1. Pressure/pain
a) in face: increases with bending forward or down; often has maxillary

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 dental pain b) in ethmoid, frontal, and sphenoid sinuses: greater in the
supine position
2. Persistent cough (worse when lying down), purulent nasal and
postnasal drainage; often lymphoid hyperplasia of pharynx 3. Fever,
nausea, fatigue
4. Sore throat, frequent clearing of throat; nasal voice
5. Nasal mucosa inflamed and boggy; TMs retracted with effusion
C. Treatment
1. Antibiotics for 10 to 14 days
a) amoxicillin or amoxicillin/clavulanate 500 mg tid or 875 mg bid b)
doxycycline 100 mg bid
c) clarithromycin (Biaxin XL) 500 mg 2 tabs qd
d) TMP/SMZ DS 1 tab bid
e) cefdinir 300 mg q12h or 600 mg qd
f) ciprofloxacin 250 to 500 mg q12h
g) clindamycin 150 to 300 mg qid
2. Adjunct therapy
a) topical decongestants (e.g., oxymetazoline nasal spray) 1 to 2 times qd
for up to 5 days b) nasal steroid, 2 sprays each nostril qd for 1 month
(e.g., fluticasone or mometasone) c) use a humidifier in the bedroom,
warm compresses on the face, and steam inhalation d) hypertonic
saline nasal spray frequently (e.g., 8 to 10 times a day) or Neti Pot 2 to
3 times a day e) increase oral fluids
f) lifestyle changes: stop smoking, wear a mask around environmental
allergens g) probiotics 1 to 2 times qd during the antibiotic course and
the next 10 days h) bromelain 100 to 450 mg tid between meals (herbal
therapy) to enhance mucolytic production and drainage
D. Referral to ENT if the symptoms do not resolve after 3 to 4 weeks of
treatment
VIII. Pharyngitis (also see Chapter 17)

A. Cause: usually viral but can be bacterial; differentiate viral from

streptococcal infection (GAS) using the rapid strep test B. Signs and

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 symptoms
1. Common presentation of GAS
a) acute-onset sore throat with tonsillar exudates
b) fever, H/A
c) tender/enlarged cervical nodes
d) may have sandpaper rash on torso and petechiae of soft palate
e) children may present with N/V and stomach pain
f) absence of cough and stuffy nose
2. Common presentation of viral pharyngitis
a) sore throat
b) coryza
c) conjunctivitis
d) cough and hoarseness
3. May also have malaise, myalgia, anorexia, difficulty swallowing
C. Diagnostic testing
1. Rapid strep test (testing not indicated if <3 years of age unless other
family members positive) 2. CBC and mono spot (if concerned about
other diagnoses)
D. Treatment
1. If a peritonsillar abscess is noted, refer immediately to ED
2. Supportive therapy with antipyretics, analgesics, throat lozenges, and
salt water gargles; encourage soft and cold foods 3. If bacterial
pharyngitis or history of rheumatic fever, start antibiotics
a) penicillin G benzathine with procaine (Bicillin CR) IM 1 time
(1) <30 lbs: 600,000 units
(2) 30 to 60 lbs: 900,000 to 1.2 million units
(3) >60 lbs: 2.4 million units
b) penicillin VK 500 mg bid for 10 days
c) amoxicillin 500 mg tid or 875 mg bid for 10 days

237
 d) with PCN allergy: azithromycin (Z-Pak) for 5 days or cefdinircefdinir
300 mg bid for 10 days or cephalexin 250 to 500 mg tid for 10 days
4. If viral pharyngitis: supportive therapy measures only
5. If the tonsils and pharynx are severely swollen, consider prednisone;
start with 30 to 50 mg qd and taper over 10 to 14 days 6. Follow-up in 2
to 3 days
E. If the symptoms are recurrent or do not resolve, refer to ENT
IX. Infectious mononucleosis

A. Cause: Epstein-Barr virus (EBV) infection contracted through contact

with oral or nasal secretions B. Signs and symptoms
1. Fever >102°F for up to 2 weeks; sore throat, enlarged tonsils with
grayish exudates, and malaise 2. Posterior cervical lymphadenopathy
(can also be in the anterior cervical, inguinal, and axillary nodes) 3.
Abdominal pain, possible splenomegaly with ↑ risk for splenic
rupture, hepatomegaly 4. Purpura or petechiae
5. Fatigue, which may persist for up to 2 months
C. Diagnostic testing
1. Mono spot (may not be positive during the first 10 days of symptoms)
2. CBC (may show decreased platelets and increased lymphocytes)
3. AST/ALT (may be elevated)
4. Consider abdominal U/S to evaluate for hepatosplenomegaly or with
unresolving pain
D. Treatment
1. Usually self-limiting illness but may last up to 2 months
2. Supportive care
a) bed rest, antipyretics, and analgesics for fever and discomfort b) good
hand hygiene, avoid sharing drinking or eating utensils and close
mouth contact c) throat lozenges and salt water gargles; encourage
hydration
3. If the tonsils and pharynx are severely swollen, prednisone may be
needed; start with 30 to 50 mg qd and taper over 10 to 14 days 4. May
consider mouth rinsing with “magic mouthwash” to decrease pain and
help improve oral intake (see Practice Pearls for ENT in this Chapter)

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 5. No contact sports or heavy lifting for up to 2 months; follow-up visit
before resuming activity 6. Antibiotics are not recommended and may
cause a maculopapular rash (especially penicillin antibiotics)
X. Influenza (also see Chapter 17)

A. Signs and symptoms

1. Sudden onset of fever (usually >102°F), malaise, myalgia, and H/A
2. Coryza, nonproductive cough, sore throat
3. Vomiting and diarrhea (occasionally in children)
4. Elderly may exhibit lower grade fever (if any), lassitude, confusion,
nasal obstruction
B. Diagnostic testing: antigen detection tests for flu A and B
C. Treatment
1. Supportive therapy: increase fluids, prevent dehydration, antipyretics
(no ASA in children), and analgesics 2. STAY HOME and rest
3. Antiviral therapy should be started within 48 hours of symptoms for
best results
a) oseltamivir (Tamiflu) adult 75 mg bid for 5 days
b) zanamivir adult 10 mg (2 inhalations) bid

P r a c t i c e Pe a r l s f o r E N T

• Aphthous ulcer treatments

• Buccal: Kenalog in Orabase or compounded clobetasol propionate

0.05% oral paste 2 to 3 times a day • Suggested “magic mouthwash”
formulas: 1 to 2 tsp swish, gargle and spit out qid prn; for all formulas,
each component is 80 ml
■ Prednisolone 5 mg/ml+nystatin susp 100,000 u/ml+lidocaine viscous
2%+diphenhydramine+Maalox/Mylanta susp+water ■ Lidocaine
viscous 2%+diphenhydramine+kaopectate
■ Prednisolone 5 mg/ml+lidocaine viscous
2%+diphenhydramine+Maalox/Mylanta susp

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• Chlorhexadine gluconate mouth rinses 1 to 2 times a day may reduce
pain • PPI for 5 to 7 days
• Consider B12 1000 mcg po qd for prophylaxis
• Usually lasts about 7 to 10 days; if the lesions worsen or ulcerative
gingivitis is noted, refer to ENT or ED emergently
• Gingivitis treatment

• Antibiotic treatment bid for 10 days Cefadroxil: 500 mg; doxycycline

100 mg • Encourage the patient to use Colgate Total or triclosan
toothpaste during exacerbation of symptoms • Chlorhexidine (i.e.,
Peridex) rinse bid (swish and spit out)
• May need pain medicine
• Refer to dentist or oral surgeon if unresponsive to treatment
• Herbal preparations for various throat disorders (not exclusive)

• Echinacea: for prophylaxis and treatment of respiratory and flu

symptoms; 1 cap bid for 10 days; do not use for >8 weeks or at all in
patient with an autoimmune disease; 2 to 4 cups of tea with Echinacea
qd may lessen cold symptoms • Hyssop: for coughs, colds, and as
expectorant; can use as tea, as gargle, and to rub on the skin prn, but
do not take if pregnant • Slippery elm: for cough and sore throat; pour
2 cups boiling water over 2 tbsp powdered bark and steep for 3 to 5
minutes and drink 1 cup tid or take 400 to 500 mg cap 3 to 4 times qd •
Honey alone or mixed with lemon will decrease cough; can be used for
patients aged >1 year
• Hypertonic saline nasal spray

• Acts to clean mucus crusts, decongests nose by shrinking membranes

to open passages, and improves nasal drainage • Mix ½ tsp sea,
pickling, or kosher salt (table salt has too many preservatives) to 6 oz
boiled or distilled water; allow to cool, and pour into a nasal spray
bottle or can purchase already prepared OTC solution (i.e., AYR-
hypertonic).
• Use frequently; keep the “homemade” saline in the refrigerator when
not using and discard any remaining liquid after 3 days and make new
solution.
• Normotonic saline nasal spray

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• Acts as a cleansing solution to remove mucus and keep nasal passages
open and moist; this improves cilia function to remove debris and
reduces postnasal drip • Saline nasal spray: mix ¼ tsp sea salt in 6 oz
of boiled water; allow to cool, and pour into a nasal spray bottle or can
purchase OTC.
• Use numerous times a day; keep the “homemade” saline in the
refrigerator when not using and throw away any remaining liquid
after 3 days and make new solution.

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CHAPTER 8

242
Cardiovascular conditions
For detailed history and physical examination, see Chapter 1.

Heart murmurs

I. Definition: turbulent blood flow through the heart as a result of one or more of the following:

A. Stenotic valve
B. Regurgitant valve (i.e., one that does not stay closed)
C. Septal defect
D. Rapid blood flow (e.g., during pregnancy and in children)
II. Description of murmurs

A. Timing (i.e., systolic or diastolic): systolic murmurs are synchronous

with the pulse and may or may not be normal; diastolic murmurs are
always abnormal

B. Quality of sound (e.g., harsh, soft, blowing, or rumbling)

C. Location best heard
D. Radiation of murmur (e.g., to the neck, left axilla, back or across the
precordium), which will be in the direction of blood flow E.
Classification of murmurs (Table 8-1 and Figure 8-1) F. Grading

1/6 Barely audible

2/6 Audible but soft
3/6 Easily audible, same loudness as S1 and S2

243
 5/6 Audible with only a rim of the stethoscope on the chest; palpable thrill
6/6 Audible with the stethoscope lifted just barely off the chest; palpable thrill

FIGURE 8-1 ​Classification of Murmurs.

Table 8-1
Classifications of Murmurs

Description Assessment Referral Points

Systolic Murmurs
Physiologic (Normal)
Grade 1/6 to 2/6, best heard
with the diaphragm
Loudest at the middle to
lower left sternal border
No radiation
May be normal in children Any previously undiagnosed murmur louder than 2/6
or in adults should be initially evaluated by an echocardiogram;
In adults, it is more depending on the results, cardiology referral may be
common with certain indicated No antibiotic prophylaxis is needed
conditions (e.g., anemia,
hyperthyroidism) No
hemodynamic changes

Aortic Stenosis
Loud, harsh crescendo- Ask about fatigue, Initial evaluation by an echocardiogram; depending on the
decrescendo murmur palpitation, DOE, dizziness, results, cardiology referral may be indicated Chest pain,
Best heard at the second right syncope, and angina dyspnea, or syncope is a critical referral point for valve
ICS with the patient leaning Radial pulse diminished replacement Antibiotic prophylaxis is no longer
forward but may be heard recommended (see Bacterial Endocarditis)
Pulse pressure may be
throughout the precordium
narrow
Frequently radiates to the
neck Sometimes the patient has
unexplained GI tract
Often associated with a thrill bleeding

244

Mitral Regurgitation
Holosystolic, blowing, often
loud
Heard best at the apex in the
left lateral position
Decreases with inspiration
Radiates to the left axilla and
occasionally to the back
Mitral Valve Prolapse
Murmur may or may not be
present; sounds like
“whoop”
A midsystolic click is best
heard over the apex with the
diaphragm
The click and murmur are
best heard while the patient
is in the sitting or squatting
position or with the Valsalva
maneuver
Diastolic Murmurs
Aortic Regurgitation
Faint and high-pitched
decrescendo, often starts
simultaneously with S2
Heard best with the
diaphragm pressed firmly at
the left third ICS, with the
patient leaning forward and
breath held in deep
expiration Radiates down
Mitral Stenosis
Diastolic rumble, best heard
at the apex with patient in
the left lateral position Best
heard with the bell of the
stethoscope
Often associated with an
opening snap, and S1 may be
louder than usual
P r a c t i c e Pe a r l s f o r M u r m u r s
insufficiency
Symptoms include fatigue, Initial evaluation by an echocardiogram; depending on the
palpitation, dizziness, DOE, results, cardiology referral may be indicated Antibiotic
syncope, and angina; prophylaxis is no longer recommended (see Bacterial
symptoms range depending Endocarditis)
on the degree of
regurgitation and HF
Left atrium usually
markedly enlarged
Symptoms include Initial evaluation by an echocardiogram; depending on the
dysrhythmias, chest pain, results, cardiology referral may be indicated Antibiotic
and anxiety prophylaxis is no longer recommended (see Bacterial
Most commonly found in Endocarditis) Encourage patients to remain well hydrated,
white, Anglo-Saxon women have adequate salt intake, and to avoid caffeine and
decongestants
Prognosis for most people is
excellent, and treatment
may not be indicated
Diagnosis is made only
with an echocardiogram;
not all clicks are significant
Minor symptoms for years, Obtain an echocardiogram and then refer to a cardiologist
then rapid deterioration Must be referred early for repair
May have associated head
Antibiotic prophylaxis is no longer recommended (see
bobbing, diaphoresis,
Bacterial Endocarditis)
carotidynia, and a quick
rise, flip, or collapsing
arterial pulse Pulse pressure
is often widened
Apical impulse displaced
down and to left
Fingernail bed pressure
reveals a pulsating red color
DOE is common Obtain an echocardiogram and then refer to a cardiologist
Poorly tolerated in pregnancy
Antibiotic prophylaxis is no longer recommended (see
Bacterial Endocarditis)
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 • To differentiate a heart murmur from a carotid bruit, simultaneously palpate the cardiac
apex while listening to the bruit; a radiating murmur will be synchronous with the apical
impulse, whereas a carotid bruit occurs somewhat later.
• A new murmur found during a sports physical examination should be evaluated by a
cardiologist before allowing the patient to participate in sports.
• A new murmur in the setting of an acute MI may indicate a ruptured papillary muscle and
impending cardiogenic shock; it is a surgical emergency.
• If the murmur starts with S1, it is probably associated with mitral or tricuspid valves; if it
does not, consider aortic or pulmonic stenosis.

Coronary heart disease (CHD)

I. Risk factors

A. CHD risk equivalents: these conditions have been associated with a

risk of a cardiovascular event (e.g., MI, CVA) equivalent to that of a
patient with known CHD; patients with these risks should be treated
as aggressively as those with known disease
1. Any noncoronary atherosclerotic disease (e.g., carotid artery disease,
PAD, AAA) 2. DM (which is also associated with other risk factors
such as obesity and dyslipidemia) 3. Chronic kidney disease (CKD),
even in mild-to-moderate stages
B. Nonmodifiable risk factors
1. Age: prevalence of any vascular disease increases significantly with
each decade of life 2. Gender
3. Family history of CHD: increased risk for a younger person with a FH
of premature CHD (MI or death from CHD in a parent or sibling
before age 50 [males] or 60 years [females])
C. Modifiable risk factors
1. Smoking: increases total cholesterol, LDL cholesterol, triglycerides,
and non-HDL cholesterol; lowers HDL cholesterol 2. Dyslipidemia:
including lipoprotein(a) [Lp(a)] in women aged <66 years 3.
Hypertension: systolic BP ≥140, diastolic BP ≥90
4. Abdominal obesity: waist at umbilicus >40 inches (males) or >35 inches
(females) 5. Psychosocial factors (e.g., stress, depression, anger)
6. Diet: specifically low in fruits, vegetables, or foods with fiber and high

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 in foods with higher glycemic indices (i.e., sugary, simple carbs) and
saturated and/or trans fats 7. Lack of or more than moderate alcohol
consumption in patients aged ≥65 years
a) “moderate” means #3 drinks a day (males) and ≤2 a day (females)
b) one drink: 12 oz beer 5 5 oz wine 5 1.5 oz 80-proof liquor
8. Lack of regular physical activity: even moderate exercise protects
against CHD and all-cause mortality
D. Other risk factors
1. Androgen deficiency in men
2. Collagen vascular diseases (e.g., RA, SLE)
3. Obstructive sleep apnea
4. Nonalcoholic fatty liver disease
E. Tools to assess risk factors for CHD (all available online)
1. Framingham risk score
(www.framinghamheartstudy.org/risk/coronary.html or
www.framinghamheartstudy.org/risk/gencardio.html) 2. Reynolds risk
score (www.reynoldsriskscore.org)
II. Risk stratification for significant disease

A. High likelihood
1. History of CHD or 1 or more risk equivalents
2. Men aged >60 years; women aged >70 years
3. Changes in hemodynamics
4. ECG changes: ST segment elevation or depression of more than 1 mm,
marked symmetric T wave inversion in multiple precordial leads (V1
through V6), or bipolar T waves in leads II, III, and aVF
B. Moderate likelihood
1. Two or more CHD risk factors (especially HTN, hyperlipidemia, and
smoking) 2. ECG changes: ST segment depression of 0.5 to 1 mm or T
wave inversion of more than 1 mm in leads with dominant R waves
C. Low likelihood
1. One risk factor

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 2. No changes in ECG (NOTE: One half to one third of patients with
angina have normal ECG readings)
III. Classification of angina

A. Stable angina occurs at predictable times (e.g., with exercise or at

stressful times) (Table 8-2) B. Unstable angina: emergent transfer to ED if
considering Acute Coronary Syndrome (see below; have the patient chew 162
to 325 mg ASA before transfer)
1. New-onset angina that markedly limits physical activity
2. Angina that is more frequent, lasts longer, or occurs with less exertion
than previously 3. Rest angina: lasts >20 minutes
4. Variant or Prinzmetal angina (reversible ST segment elevation on
ECG)
C. Acute coronary syndrome (ACS)
1. Unstable angina
2. Non–ST-elevation MI (NSTEMI)
3. ST-elevation MI (STEMI)
IV. Diagnostics

A. Initial
1. ECG (keep in mind that the initial ECG may be normal, even with
acute MI) 2. Chemistry profile (be sure it includes serum magnesium)
3. Fasting lipid profile
4. Consider high-sensitivity C-reactive protein (hs-CRP) if no known
CHD; it can help with risk stratification 5. Low-level stress test in men
and cardiolyte nuclear stress in women (regular stress test is only 42%
accurate in women). An abnormal stress test is defined by the
following:
a) inability to exceed beyond stage II or 6 minutes on the standard Bruce
protocol or
b) presence of ischemic symptoms and/or signs (characteristic angina
pain or ≥1-mm ST segment changes in 2 or more leads) or
c) inappropriate systolic BP and/or an inability to meet or exceed 85% of
the predicted maximal heart rate or

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 d) ventricular dysrhythmias
6. Echocardiogram
B. Definitive workup
1. Cardiac catheterization
2. Thallium studies or chemical (e.g., dipyridamole or dobutamine) stress
test
V. Treatment

A. Consult a cardiologist if angina is new onset or has changing

characteristics B. Medications (see Table 8-3)
1. Nitrates are used for acute treatment and prevention
2. If necessary, the practitioner may prescribe a beta-blocker, calcium
channel blocker, or both for prevention 3. ASA 81 mg hs to reduce the
risk of MI or CVA
C. Dietary therapy: after a review of the lipid profile, select an
appropriate diet; consider calorie reduction for overweight or obese
patients D. Exercise: after clearance by a physician, exercise 65% to
75% of the maximum for the age E. Smoking cessation
F. Consider a statin (see Table 8-10) to reduce the risk of MI and CVA,
even if cholesterol levels are not elevated
Table 8-2
Classification of Angina

Class Activity/Onset Limits to Normal Activity

I Prolonged exertion None
II* Walking 2 blocks Slight
III* Walking <2 blocks Marked
IV Minimal or rest Severe
*A practical differentiation between class II and III is the ability to walk two blocks or climb one flight of stairs.

P r a c t i c e Pe a r l s f o r A n g i n a

• Do not obtain a stress test with unstable angina (Acute Coronary Syndrome).

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• “Chest pain”

• Women often have atypical angina: vague, but descriptive;

unexplained SOB; exhaustion; “full” feeling or discomfort; indigestion;
profound fatigue; disturbances in sleep or thinking; often occurs with
arm activities.
• A constant aching pain that might occur in the substernal area and
persist all day or a pain that is present only in one position and not in
others is usually not caused by heart disease.
• Pain over the apical region of the heart or over the right anterior chest
region is not typical of coronary artery pain.
• A fleeting, momentary pain in the chest described as a needle jab or
stick, lasting only 1 to 2 seconds, is not heart pain.
• A BP cuff left on and inflated too long may mimic the left arm pain of a
patient with a cardiac disorder.
• If the patient is able to localize the pain with a finger or two to a small
region, it is usually not cardiac in nature; cardiac pain tends to be
diffuse.
• Look for associated symptoms with chest pain; patients with AMI frequently complain of
feeling unusually tired for months or weeks preceding MI.
• Have the patient keep a diary of symptoms and precipitating events; refer if the patient
continues to have symptoms, even with a normal treadmill.
• Medications

• Do not give isosorbide mononitrate (Imdur, ISMO, or Monoket) as

q12h dosing (Table 8-3); it is designed with an abstinence period to
prevent tachyphylaxis.
Table 8-3
Medications for Angina

Medication Advantages and Disadvantages Examples

Nitrates Reduce angina and improve exercise tolerance in
stable angina
Decrease the risk of AMI in unstable angina
Extended-, sustained-, and controlled-release forms
are for prevention; they are not used to treat an acute
angina episode Most require a 6-to 8-h period of
abstinence to prevent tachyphylaxis
Disadvantages include tolerance, H/A, hypotension,
and need to regularly space doses
Nitroglycerin sublingual 0.4 mg (range 0.3-0.6
mg) q5min, up to 3 tabs or 3 sprays; transfer
to ED for further evaluation Nitroglycerin
extended-release capsule 2.5-18 mg tid-qid
Nitroglycerin ointment (2%, 15 mg/in) 1⁄2-3 in
bid, 6 h apart
Nitroglycerin transdermal patch 0.2-0.8 mg
worn for 12 h qd
Isosorbide dinitrate sustained-release cap/tab
40-80 mg q8-12h

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 Isosorbide mononitrate (Monoket 10-20 mg or
ISMO 20 mg given bid, 7 h apart or Imdur 60-
120 mg given once daily)

Beta-blockers Improve exercise tolerance and reduce angina in Noncardioselective agents

stable angina
Reduce angina and the risk of AMI in unstable
angina
Particularly helpful if the patient has exercise-
associated tachycardia with angina Disadvantages
include bronchoconstriction, AV block, reduced
contractility (may induce HF), and changes in blood
lipids
Propranolol immediate-release 20-80 mg tid-
qid or extended-release (Inderal-LA) 80-320
mg qd Nadolol 40-240 mg qd
Cardioselective Agents
Atenolol 50-100 mg qd
Metoprolol tartrate (Lopressor) 50 mg bid or
extended release (Toprol XL) 100 mg qd;
maximum dose for both is 400 mg qd

Calcium Given if contraindications to or adverse reactions Nifedipine (Procardia XL) 30-90 mg qd

channel with beta-blockers or added to treatment if beta- Diltiazem extended-release cap 120-480 mg qd
blockers blockers alone are not successful Improve exercise or tab 180-360 mg qd
tolerance and reduce angina in chronic angina
Nicardipine 20-40 mg tid
Reduce angina in unstable angina (especially
nicardipine) Verapamil immediate-release 80-120 mg tid or
(Covera-HS) 180-540 mg hs Amlodipine 5-10
Disadvantages include hypotension, AV block, mg qd
reduced contractility (verapamil, diltiazem,
nifedipine may induce HF), constipation, edema, and
tachycardia with some agents

• Primary prevention with ASA 81 mg

■ Moderate-to high-risk patients (individuals with a 10-year risk of first
CHD event >10%): decision made on an individual basis for those in
whom the benefit is likely to exceed the risk of major bleeding; also
consider whether to add ASA to other preventative measures such as
statins ■ Low-risk patients (individuals with a 10-year risk of first CHD
event <10%): do not recommend because the benefit is unlikely to
exceed the risk of major bleeding • NTG sublingual tablets are good
until the expiration date on the bottle, as long as they are kept in the
original bottle, tightly capped, and at room temperature.
• Omega-3 fatty acids can decrease triglycerides, inhibit blood clotting,
and may decrease dysrhythmias associated with sudden cardiac death;
encourage two servings of fish weekly (primarily salmon, tuna,
mackerel, herring, or sardines); fish oil supplements do not improve
cardiovascular outcomes in high-risk patients.
• NSAIDs (except ASA)
■ Limit use in cardiac patients; use the lowest dose for the shortest time.
■ Naproxen has the least cardiovascular risk; avoid selective COX-2 meds
(e.g., celecoxib) and diclofenac.

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• Education

• Teach the patient about medication(s) and the expected side effects.
• Teach the patient and family when to call 911 or the emergency medical
system.
• Teach the patient how to read labels and calculate fat intake.
• Encourage family CPR training.
• Encourage the patient to stop smoking; the risk of recurrent MI
decreases 50% within 1 year of cessation and normalizes to that of a
nonsmoker within 2 years.
• For chest pain differential diagnoses, see Table 8-4
Table 8-4
Chest Pain Differential Diagnosis

Description Confirm by Exclude by

Acute MI or Acute Coronary Artery Insufficiency
Severe, oppressive, constricting retrosternal ECG changes Usually by normal
discomfort; often radiates to the left shoulder and Serial cardiac enzymes serial ECGs or
down the left arm (on the inside of the arm) Onset observation in the
is usually at rest hospital
Lasts >30 min Normal serial
Often accompanied by anxiety, restlessness, cardiac enzymes
diaphoresis, or dyspnea (if no MI)

Prior history of angina or MI

Levine sign (holding fist to chest)
Possible dysrhythmias or HF

Aortic Dissection
Very abrupt, tearing pain in the anterior or May be found on an echocardiogram or Normal
posterior chest, frequently between the shoulders; abdominal U/S mediastinum on
often migrates to the arms, abdomen, and legs Usually found with angiography, CT scan, CXR
Pulse deficits or MRI
Shocky but hypertensive
Possible neurological changes (especially in the
legs)
Diastolic HTN with aortic diastolic murmur

Pericarditis
Pleuritic chest pain, often worse in the supine Typical ECG: concave ST segment Normal ECG
position, better when sitting up; referred to the elevation in all leads except aVR and V1 Normal
trapezius ridge Pericardial friction rub echocardiogram
Pericardial friction rub
Often associated with disease (e.g., viral infection, Absence of friction
Echocardiography
recent MI, connective tissue disease) rub

Pulmonary Embolism
Pleuritic chest pain or sudden dyspnea, V/Q scan or pulmonary angiography or Normal V/Q scan

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apprehension, and palpitations both Observation in
Occasionally, acute nonpleuritic chest “pressure” ECG changes typical of PE (right hospital
with hemoptysis ventricular strain)
Clinical signs of DVT
Factors predisposing to venous thrombosis (e.g.,
postpartum, use of OCs, prolonged bed rest, HF)

Pneumothorax or Pneumomediastinum
Sudden dyspnea or retrosternal pain, cough, and CXR Normal CXR
lateral chest pain (including lateral
Diminished breath sounds with possible view)
mediastinal shift
Possible history of asthma, COPD, or chest trauma
Possible subcutaneous emphysema (skin “crackles”
on touch)

Pneumonia
Usually pleuritic chest pain with cough and fever CXR Normal CXR (>24
Dull to percussion (affected area) h after symptom
onset)
A to E changes (affected area)

Esophageal Spasm
Substernal constricting pain, often at the time of Barium swallow Normal
swallowing Endoscopy esophageal
History of dysphagia manometry
Esophageal manometry
Pain related to cold and carbonated drinks or food

Esophagitis
Heartburn and acid brash Endoscopy Normal
Worse when bending over or supine Biopsy endoscopy and
biopsy or UGI
Better with antacids UGI series series

Biliary Colic
Constant epigastric or right upper quadrant pain; Clinical history Absence of
may extend to the back Abdominal U/S or HIDA scan gallstones and/or
Often positive Murphy sign normal HIDA scan

Lasts 15 min to 6 h
Associated with N/V; possible fever

Acute Pancreatitis
Severe epigastric or periumbilical pain radiating to Elevated serum amylase and lipase Normal amylase
the back and lipase
Clinically looks very sick
Associated with N/V
Tender epigastrium
History of alcohol use or gallstones; may be
associated with high triglycerides and DM

Peptic Ulcer Disease

Epigastric postprandial discomfort Upper GI series or endoscopy Normal GI series
Often relieved with antacids or food or endoscopy

May respond to antacid or H2 antagonist trial

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 Musculoskeletal Chest Wall Pain/Costochondritis
Sharp pain, usually worse with deep breath or Reproducible pain with pressure along the Pain not
certain movements (e.g., twisting) Often associated costosternal and/or paravertebral junctions reproducible with
with back pain, which is worse in the supine (often T8-10; T7 level is at the low end of pressure to the
position scapulae) painful area
Often associated with a history of lifting or moving
a heavy object

12-lead ECG

I. Description

A. See Figure 8-2 for normal 12-lead ECG

B. Ischemia, injury, and infarction of the ventricle are reflected in the 12-
lead ECG; each area of the ventricle is reflected in certain leads. With
myocardial infarction, there is a strong correlation between the leads
showing changes and the location of actual disease. See Tables 8-5 and
8-6 for acute changes.
C. Generally, progressive changes on ECG tracing indicate acute MI
(AMI)
1. T waves initially heighten and become peaked
2. ST segments elevate
3. T waves become inverted
4. Q waves form, and R waves lose some of their height (non–ST-
elevation MIs [NSTEMI] do not develop Q waves)
D. It is important that the nurse practitioner treat the patient and not the ECG.
Refer for clinical symptoms. Do not wait for ECG changes.
II. Emergency treatment of suspected AMI

A. Administer oxygen
B. Start IV line (if equipment is available)
C. Have the patient chew 162 or 325 mg of ASA (R/O aortic dissection or
peptic ulcer disease) D. Transport to the hospital by advanced life
support means immediately

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 FIGURE 8-2 ​12-Lead ECG. Because 12-lead ECG tracings do not look
alike, it is important to know the criteria for “normal”:
• Sinus rhythm
• Normal measurements (i.e., PR: 0.12 to 0.2 sec, QRS: 0.04 to 0.1 sec,
and QT: 0.32 to 0.44 sec)
• All ST segments level with baseline (i.e., no depression or elevation)
• All T waves usually upright except aVR; may be inverted in lead III or V1
• QRS complex in leads I, II, and aVF upright
• Normal R wave progression: in looking at leads V1 through V6, the QRS
complex becomes more positive than negative in either V3 or V4
Any deviation from these criteria will create an abnormal ECG, which is
not necessarily life threatening.
Table 8-5
Acute Changes on 12-Lead ECG

Acute
ECG Findings
Changes
Ischemia ST segment depression >1 mm and T wave inversion (if the inversion is deeply
symmetrical, it is more significant)
Injury ST segment elevation >1 mm is generally significant
Necrosis Q waves are signs of necrosis; to be diagnostic of MI, the Q wave must be ≥0.04 sec
wide or > one quarter of the total height of the QRS complex

Table 8-6
Location of Changes on 12-Lead ECG

Leads Artery Involved

Left Ventricle
Anterior V1, V2, V3, V4 Left anterior
descending coronary
artery
Inferior II, III, aVF Usually RCA but
may be left
circumflex
Lateral I, aVL, V5, V6 Left circumflex

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 Posterior V1, V2 (acute changes include tall R wave and RCA
ST segment depression)
Right Ventricle
Right ventricular MI V4 on the right side of the chest (V4R) (acute RCA
(associated with inferior change is ST segment elevation >1 mm)
MI)

Heart failure
I. Description

A. Heart failure is a chronic illness characterized by progressive

deterioration and punctuated by periodic symptomatic exacerbations
B. Causes: results in failure of the heart to keep up with the metabolic
demands of tissues; possible etiologies include the following:
1. Ischemia (i.e., CHD)
2. Valvular: aortic stenosis, mitral regurgitation
3. Toxins: alcohol, chemotherapy
4. Heart muscle disease
a) dilated cardiomyopathy
b) hypertrophic cardiomyopathy
c) inflammation (i.e., viral cardiomyopathy)
5. Severe lung disease, OSA
6. DM
7. Congenital
8. Rheumatological
II. Clinical manifestations

A. Systolic dysfunction (HF with reduced ejection fraction [EF]) occurs

when the heart muscle is dilated and thin walled; low EF (e.g., <40%)
occurs because of reduced contractility of the weakened muscle; often
results from CHD or MI B. Diastolic dysfunction (HF with preserved
EF) is associated with a hypertrophied myocardium with elevated
filling pressures; the EF is >50%. Diastolic dysfunction is often the
result of HTN; it is also found with ischemic heart disease,
hypertrophic obstructive cardiomyopathy, DM, and chronic kidney
disease.

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 C. Left ventricular versus right ventricular failure
1. Left ventricular failure is associated with reduced cardiac output
systemically and associated pulmonary congestion; it is often the result
of CHD, MI, valvular heart disease, cardiomyopathy, and/or HTN
2. Right ventricular failure is associated with systemic congestion (e.g.,
hepatic congestion and peripheral edema); right ventricular failure is
usually the result of left ventricular failure (in which case, there may
be pulmonary congestion too) and may also be the result of pulmonary
HTN, right ventricular MI, or COPD (HF caused by COPD is called cor
pulmonale)
D. Acute versus chronic
1. Acute (days to weeks): mainly SOB at rest and/or with exertion; also
orthopnea 2. Chronic: PND, fatigue, anorexia, abdominal distention,
and peripheral edema may be more pronounced than dyspnea
III. Signs and symptoms

A. Symptoms
1. Exertional dyspnea
2. Exercise intolerance
3. Cough, worse in the recumbent position
4. Nocturnal symptoms
a) orthopnea: difficulty breathing beginning less than 1 minute after
lying down b) paroxysmal nocturnal dyspnea: occurs 2 to 4 hours into
sleep
5. Abdominal discomfort
6. Fatigue or altered mental status
B. Signs
1. Crackles (specific but not a very sensitive finding; clear lung fields tell
very little about the fluid status of the heart) 2. Increased JVD (best
physical finding for determining the fluid status) (see Chapter 1,
Physical Examination, VI, E) 3. Laterally displaced PMI
4. Peripheral edema
5. Hepatomegaly and ascites

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 6. May have S3 heart sound
IV. Diagnostics

A. Not all patients will have evidence of fluid retention

B. There is no single diagnostic test for HF. Tests (e.g., labs, ECG) are
done to determine the degree and type of HF and if there is a
reversible cause; for recommended testing, see also Table 8-7.
V. Classification

A. NYHA classification describes the severity of symptoms; ejection

fraction (EF) does not correlate with the class

I No limitations to physical activity

II Symptoms with usual activities
III Symptoms with minimal activities
IV Inability to carry out physical activity without discomfort; symptoms at rest

B. American College of Cardiology (ACC)/American Heart Association

(AHA) guidelines classify patients at risk for having HF

Stage Patient description

A High risk for developing heart HTN
failure CAD

258

B Asymptomatic heart failure
C Symptomatic heart failure
D Refractory end-stage heart failure Marked symptoms at rest despite maximal medical
DM
Family history of cardiomyopathy
Previous MI
Left ventricular systolic dysfunction
Asymptomatic valvular disease
Known structural heart disease
Shortness of breath and fatigue
Reduced exercise tolerance
therapy

VI. Treatment

A. HF should be managed in collaboration with a physician

B. Risk reduction (all stages)
1. Weight reduction if the patient is obese
2. Control lipids, HTN, and DM
3. Maintain fluid balance: sodium restriction and daily weights
a) stages A & B: <2 to 3 g sodium daily
b) stages C & D: <2 g sodium daily
C. Stop smoking and ETOH consumption
D. Encourage regular exercise (e.g., walking) to tolerance
E. Consider evaluation for OSA (patients rarely report excessive daytime
sleepiness) F. Take medications (according to the ACC/AHA
guidelines) (Table 8-8)
Table 8-7
Additional Recommended Testing for HF Signs and Symptoms

Test Finding Possible Diagnosis

ECG Acute ST-T Ischemia
changes Thyroid disease
Atrial fibrillation HF due to slow rate
Bradycardia Depressed LV function
Previous MI Diastolic dysfunction
LVH
Troponin T or I Elevated Myocardial ischemia/injury
CBC Anemia Decreased O2 carrying capacity
UA Proteinuria Casts Nephrotic syndrome Glomerulonephritis
Serum Elevated Renal failure
BUN/creatinine
Serum albumin Decreased Increased extravascular volume or poor nutrition

259
 TSH Abnormal Hypothyroidism or hyperthyroidism
Echocardiogram Abnormal Systolic or diastolic dysfunction
Valvular heart disease
Pulmonary HTN
Coronary heart disease
CXR Abnormal Primary pulmonary disease HF, septal defects, or mitral or
Cardiomegaly aortic valve stenosis

Table 8-8
​Medications for the Treatment of Heart Failure

Stage Suggested Medical Therapy

A Risk reduction measures
B ACE* (ARB*, if intolerant to ACE)
• Patients with recent or remote MI or acute coronary syndrome and EF <40%
• All patients with decreased EF (<40%)

Beta-blocker
• Patients with recent or remote MI or acute coronary syndrome and EF <40%
• All patients with decreased EF (<40%)
• Carvedilol (Coreg) 3.125 mg bid, doubling q2wk to 25 mg bid if tolerated • Metoprolol extended release
(Toprol XL) 12.5-25 mg qd, doubling q2wk to 200 mg qd if tolerated

Statin
• All patients with recent or remote MI or acute coronary syndrome

C ACE* (or ARB*, if intolerant to ACE): all patients

Beta-blocker: all patients
• Carvedilol (Coreg) 3.125 mg bid, doubling q2wk to 25 mg bid if tolerated • Metoprolol extended release
(Toprol XL) 12.5-25 mg qd, doubling q2wk to 200 mg qd if tolerated

Loop diuretic*
• Patients with NYHA class II-IV HF
• Only as needed to correct or maintain fluid balance

Aldosterone antagonist: monitor serum K+ and creatinine monthly for 9 mos, q3mo for 9
mos, and then periodically
• All patients with NYHA Class III-IV symptoms and who have EF <35%, as long as eGFR >30 ml/min and K+ <5
mEq/L
• Spironolactone 12.5-25 mg qd
• Eplerenone 25 mg qd

Hydralazine/nitrates
• Persistently symptomatic African-Americans; NYHC class III-IV despite taking ACE, beta-blocker, and
aldosterone antagonist • Any patient with current or prior symptoms of systolic HF who cannot take or is
intolerant to ACE or ARB
• Hydralazine/isosorbide dinitrate 37.5 mg/20 mg tid

Digoxin: may be beneficial in systolic HF to decrease hospitalizations

• 0.125-0.25 mg qd (0.125 mg if age >70 yrs or impaired renal function)

D Referral to a heart failure center or cardiologist for management

*See Tables 8-15 and 8-16 for dosing and precautions.

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 P r a c t i c e Pe a r l s f o r H e a r t F a i l u r e

• The two listed beta-blockers have been shown to be effective in decreasing the risk of death
in HF; this is not a class effect.
• For patients taking aldosterone antagonists:

• Counsel them to avoid foods high in potassium (see Appendix A) and

NSAIDs.
• Check serum K+ and renal function 2 to 3 days and again at 7 days after
starting the med and then at least monthly for 3 months, followed by
q3mo. Addition of or increase in the dosage of ACE or ARB starts a
new monitoring cycle.
• Statins should not be prescribed for HF treatment to improve clinical outcomes but only if
otherwise indicated.
• Calcium channel blockers are not recommended as routine treatment for systolic HF; they
have shown no functional or survival benefit in patients with HF. Amlodipine may be used
for comorbid HTN or ischemic heart disease because it is generally well tolerated and safe.

Ambulatory dysrhythmias
As a general rule, significant dysrhythmias require oxygen therapy.

Fast rhythms

I. Sinus tachycardia

A. Description: normal components with a rate of >100/min

B. May be normal in children but never found in adults without a cause
(e.g., fear, pain, anxiety, fever, HF, hypoxia, hyperthyroidism,
hypotension, AMI, volume depletion, shock) C. Treatment
1. Treat the cause
2. Requires appropriate diagnostic workup after analysis of the history
and possible causes
D. Referral: if unable to detect and treat the cause
II. Atrial fibrillation

A. Description: irregular ventricular rhythm with absence of P waves

261
 B. May be paroxysmal (intermittent or lasting <7 days), persistent (lasting
>7 days to 1 year), or permanent (lasting >1 year)
C. Increased risk with CHD, COPD, AMI, hypoxia, holiday heart
syndrome (associated with excessive alcohol bingeing),
hyperthyroidism, hypomagnesemia, obstructive sleep apnea D.
Treatment
1. Depends on the ventricular rate and how long the rhythm has been
present; controlling symptoms is important, but reducing the risk of
CVA is critical
2. With a rapid rate, may try: a beta-blocker or diltiazem; digoxin may be
used, primarily in a sedentary patient aged >80 years 3. Consider
emergency transfer to ED if the patient is hemodynamically unstable
E. Referral
1. Any new onset of atrial fib should be urgently referred to a cardiologist
for evaluation 2. Anticoagulation therapy should be started as soon as
possible after diagnosis with high-risk patients, as documented by a
CHA2DS2-VASc score of 2 or higher (Table 8-9); consider
anticoagulation with a score of 1. Treatment choices include warfarin
or newer anticoagulants (see Tables 9-2 and 9-4).
III. Paroxysmal supraventricular tachycardia

A. Description: sudden onset of regular rhythm with narrow QRS

complexes and a rate usually >150/min B. Causes include CHD,
medications, mitral valve prolapse, hyperthyroidism, digoxin toxicity,
and excessive stimulants (e.g., caffeine, ETOH, nicotine, drugs such as
cocaine) C. Treatment: rhythm may terminate spontaneously or
require therapy to stop
1. Simple measures to try include Valsalva maneuver and cough
2. Possible medications include adenosine, verapamil, diltiazem,
propranolol 3. Consider emergency transfer to ED if the patient shows
signs of hemodynamic instability
D. Referral: new onset should be referred to a physician (consider an
electrophysiologist, if available) for evaluation and treatment plan
Table 8-9
CHA2DS2-VASc Score

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 Clinical Finding Points
Diagnosed heart failure (any type) 1
HTN, treated or untreated 1
Age 65-74 yrs 1
Diabetes 1
Vascular disease (e.g., MI, PAD, aortic plaque) 1
Female sex 1
Previous CVA or TIA 2
Age ≥75 yrs 2
For a score of ≥2, anticoagulation therapy should be started as soon as possible. Consider anticoagulation with a score of 1.

Slow rhythms (sinus bradycardia or AV blocks)

I. Description: ventricular rate <60/min; if <40/min, consider the presence of an AV block II.
Causes include medications, hypothyroidism, vagal response, AMI, and athletic heart (i.e.,
patient in a very good physical shape)
III. Treatment

A. Attempt to treat the cause if possible (e.g., decrease beta-blocker dose)

B. If the patient is symptomatic (e.g., hypotensive, altered mentation,
SOB, chest pain), consider giving atropine 0.5 mg rapidly IV (if
available)
IV. Referral

A. If unable to detect and treat the cause (and the patient is stable), refer
to a cardiologist B. If associated with a syncopal episode or if the
patient is symptomatic or if the ventricular rate is <40/min, emergency
transfer to the ED

Premature ventricular complexes (PVCs)

I. Description: wide QRS complexes interspersed in normal rhythm; may be occasional to

frequent II. Causes include AMI, CHD, electrolyte imbalance, hypoxia, and medications III.
Treatment

A. Often do not require treatment, but development of ventricular

tachycardia is a concern (three or more PVCs in a row at a rate of
>100/min) B. PVCs should not be treated unless determined significant
by a physician C. Verify normal serum potassium and magnesium
levels
IV. Referral: if ventricular tachycardia develops (even in brief runs), transfer to ED via
emergency transport

Hyperlipidemia

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I. Description: Hyperlipidemia is a leading cause of mortality and morbidity, especially when it
is associated with coronary heart disease II. Screening recommendations

A. Males aged ≥35 years (or 21 to 35 years with an increased risk of CHD)
and females aged ≥21 years with an increased risk of CHD: fasting
lipoprotein profile (total, LDL, and HDL cholesterol levels; triglyceride
levels) q5yr B. There is no consensus on screening in pediatrics
1. Consider in an obese child with other risk factors (e.g., strong family
history of DM, CVD, or HTN) 2. Abnormal values are noted below;
these have not been validated as accurate predictors for accelerated
atherosclerotic or cardiovascular disease
a) total cholesterol: >200 mg/dl
b) LDL-C: >130 mg/dl
c) non-HDL-C: >145 mg/dl
d) triglycerides: child aged 0 to 9 years, >100 mg/dl; 10 to 19 years, >130
mg/dl e) HDL-C: <40 mg/dl
III. Secondary causes of hyperlipidemia: Need to be ruled out before beginning lipid-lowering
therapy

A. Elevated LDL
1. Diet: saturated or trans fats, weight gain, anorexia
2. Drugs: diuretics, cyclosporine, glucocorticoids, amiodarone
3. Diseases: biliary obstruction, nephrosis, hypothyroidism, obesity
B. Elevated triglycerides
1. Diet: weight gain, low-fat diet, high intake of refined carbohydrates 2.
Excessive ETOH consumption (>2 drinks qd [females] or 3 drinks qd
[males]; one drink = 12 oz beer = 5 oz wine = 1.5 oz 80-proof liquor) 3.
Drugs: oral estrogen, glucocorticoids, bile acid sequestrants, retinoic
acid, protease inhibitors, anabolic steroids, raloxifene and tamoxifen,
beta-blockers (except carvedilol), thiazides 4. Diseases: nephrosis,
chronic renal failure, poorly controlled DM, hypothyroidism, obesity
IV. Treatment goals

A. LDL: depends on patient age, presence/absence of clinical

arteriosclerotic cardiovascular disease (ASCVD), and LDL levels B.
HDL: >40 mg/dl (males) or >50 mg/dl (females)

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 C. Triglycerides: <150 mg/dl
1. If triglycerides are elevated, LDL is small and dense regardless of its
value 2. A trigs ÷ HDL value of >3 indicates presence of insulin
resistance
V. Treatment

A. Therapeutic lifestyle changes should be emphasized for every patient,

regardless of other treatments
1. Diet therapy: should be tried for 3 months before medications are
started (unless CHD exists or the patient is diabetic)
a) AHA recommends a “heart-healthy diet” rich in vegetables, fruits,
fiber-rich whole grains, lean meats, and poultry; fish at least twice a
week; fat-free or 1% dairy products; low in saturated and trans fats,
cholesterol, sodium, and added sugars b) Mediterranean diet:
decreases the relative risk of cardiovascular events by 30% in 5 years
(similar to some statins)
2. Regular exercise (e.g., walking 30 minutes 5 times a week)
3. Weight loss, if applicable
B. LDL (from 2013 ACC/AHA Blood Cholesterol Guideline)
1. The focus is on treatment of cholesterol to decrease ASCVD risk using
the appropriate intensity of statin therapy in those most likely to
benefit (no improved ASCVD outcomes by simply meeting a specific
LDL goal) 2. The Pooled Cohort Equations are recommended to
estimate 10-year ASCVD risks for CHD and CVA in patients aged 45
to 75 years who do not have clinical ASCVD (e.g., acute coronary
syndrome; history of MI, stable/unstable angina, CABG or other
arterial revascularization, CVA, TIA, or PAD). See
http://my.americanheart.org/cvriskcalculator.
a) if the patient is already on a statin, use pretreatment cholesterol values
b) consider statins if the 10-year risk is ≥7.5%
3. Nonstatin therapies do not acceptably decrease ASCVD risk compared
with the potential for adverse outcomes
C. Statin benefit groups (see Table 8-10 for High-, Moderate-, and Low-
Intensity Statin Therapy)
1. All patients aged ≤75 years with clinical ASCVD: high-intensity statin

265
 therapy should be initiated/continued unless contraindicated;
moderate-intensity therapy is the second option
2. Patients aged ≥21 years with no clinical ASCVD
a) LDL ≥190 mg/dl: high-intensity statin therapy; often needs nonstatin
cholesterol lowering medication as well (Table 8-11) b) If the patient is
>75 years of age: evaluate the potential for ASCVD versus the risk of
adverse effects; it is reasonable to start or continue moderate-intensity
statin therapy for patients who can tolerate it
3. Patients aged 40 to 75 years with DM: high-intensity statin therapy; in
patients aged <40 or >75 years, individualize statin therapy according
to the benefits of ASCVD risk reduction versus possible side effects or
drug interactions 4. LDL 70 to 189 mg/dl with no DM: start statin
therapy depending on the 10-year ASCVD risk ≥7.5% (see
http://my.americanheart.org/cvriskcalculator) 5. For patients with NYHA
class II-IV HF or undergoing hemodialysis: consult with or refer to a
cardiologist regarding statin therapy
D. Monitoring statin therapy
1. Obtain fasting lipid panel before starting, in 4 to 12 weeks (determines
patient adherence), and then q3-12mo as clinically indicated 2. Obtain
baseline ALT/AST before starting therapy; if normal, further hepatic
monitoring is not needed unless hepatotoxicity signs/symptoms occur
(e.g., unusual fatigue, abdominal pain, dark urine) 3. Measure CK only
with complaints of muscle symptoms (e.g., pain, tenderness, weakness,
cramps) 4. If also using nonstatin cholesterol lowering medications,
more intensive monitoring may be indicated
E. For muscle pain associated with statins, consider the following:
1. Stop statin if CK level is >10 times the normal or if the symptoms are
intolerable 2. Try lowering the dose or give less frequently (e.g.,
rosuvastatin or atorvastatin q2-3d)
3. Change to pravastatin or low-dose rosuvastatin
4. Correct low vitamin D or hypothyroidism (both can cause myalgias)
F. Statin administration
1. Give statins bid if insomnia occurs (split the tablet in half and take bid)
2. Atorvastatin and rosuvastatin may be given any time of the day;

266
 others work better if given in the evening.
3. Do not give simvastatin >40 mg qd or >20 mg qd if the patient is on a
calcium channel blocker
G. Use statins cautiously with fibrates because rhabdomyolysis may
occur (consider this with myalgias, dark urine, and CK level ≥5 times
the upper limit of normal)
Table 8-10
High-, Moderate-, and Low-Intensity Statin Therapy

Therapy Effectiveness Statins

High-intensity therapy Lowers LDL, on average, approximately ≥50% when taken daily Atorvastatin 80 mg*
Rosuvastatin 20 (40)
mg

Moderate-intensity Lowers LDL, on average, approximately 30%-49% when taken Atorvastatin 10 (20) mg
therapy daily Rosuvastatin (5) 10 mg
Simvastatin 20-40 mg
Pravastatin 40 (80) mg
Lovastatin 40 mg
Fluvastatin 40 mg bid

Low-intensity therapy Lowers LDL, on average, by <30% when taken daily Pravastatin 10-20 mg
Lovastatin 20 mg

*Decrease
dose to 40 mg qd if 80 mg is not tolerated.
Dosages in italics are FDA approved but not tested in the trial reviewed for the guidelines.

P r a c t i c e Pe a r l s ( f o r n o n s t a t i n t h e r a p y )

• Lp(a)

• Lp(a) and apolipoprotein B should be measured in women with

premature CHD (i.e., <60 years of age), even if the lipid profile is
normal.
• At present, consider screening and treating for elevated Lp(a) in
patients with the following:
■ CHD and no other identifiable dyslipidemia
■ Strong family history of CHD and no personal history of dyslipidemia

267
■ Elevated cholesterol refractory to statins
• Niacin (2 to 4 g/day) will decrease Lp(a) and LDL but has not been
shown to decrease outcomes such as death or MI; statins and bile acid
sequestrants do not decrease Lp(a) levels.
• Niacin (see Table 8-11): to decrease the frequency and severity of skin side effects

• Take with food or take ASA 325 mg 30 minutes before niacin.

• With extended-release niacin, increase the dose by 500 mg q1-2wk to a
maximum of 2000 mg qd.
• With immediate-release niacin, start with 100 mg tid and titrate up to
3000 mg qd, divided in 2 to 3 doses.
• Bile acid sequestrants (BAS) (see Table 8-11)

• Do not use BAS or statins for the treatment of isolated elevations of

VLDL because both may increase VLDL levels.
Table 8-11
Nonstatin Therapy

Medication Initial Dose Monitoring

Bile Acid Sequestrants
Cholestyramine 4 g tid-qid Obtain fasting lipid profile before starting, in 3 mos, and q6-12 mos
(Questran, 6 g qd thereafter.
Cholybar) Discontinue if triglycerides exceed 400 mg/dl.
3 tablets bid or 6
Colestipol tablets qd with food
(Colestid)
Colesevelam
(Welchol)

Fibric Acid Derivatives (Fibrates)

Gemfibrozil 600 mg bid ac Monitor LFTs and lipids at the start of therapy, at 12 wks, and periodically
(Lopid) thereafter; stop if ALT >100 units/L.
Gemfibrozil: avoid if creatinine >2 mg/dl and use cautiously with hepatic
impairment*
Should not be used with statins (increased risk of rhabdomyolysis)

Fenofibrate 67-200 mg qd Monitor renal status (serum creatinine and eGFR) before starting, in 3 mos,
and q6mo thereafter. Do not use if eGFR <30 ml/min; do not exceed 54
mg/day if eGFR 30-59 ml/min.
May use with low-or moderate-intensity statin only if the benefits exceed
the potential risk for side effects or if triglycerides >500 mg/dl.

Niacin
Niacin 1-3 g tid with or after Obtain baseline ALT/AST, FBG or A1c, and uric acid before starting, during
(nicotinic acid) meals dose increases, and q6mo thereafter.
Do not use if ALT/AST >2-3 times the normal or with gout or persistent
hyperglycemia.

268
 Use cautiously with renal impairment and do not use with active liver
disease.

Niacin, 500 mg hs, adjust

extended dose by 500 mg qd at
release 4-wk intervals
(Niaspan)

Miscellaneous Medications
Ezetimibe 10 mg qd Monitor lipids periodically.
(Zetia) Do not use with moderate-to-severe hepatic impairment*.

Omega-3 4 caps qd Monitor lipids periodically.

capsules Used when triglycerides ≥500 mg/dl
(Lovaza,
Vascepa)

*Includes
history of liver disease, consuming substantial quantities of ETOH, and/or unexplained elevations in ALT and AST.

• Constipation resulting from BAS can be reduced by increasing the dose

slowly and by concomitant administration of psyllium (Metamucil) or
methylcellulose (Citrucel).
• OTC supplements

• Omega-3 fatty acids can lower lipids; encourage two servings of fish per
week (salmon, tuna, mackerel, herring, or sardines); OTC fish oil
capsules may lower values but have not been shown to decrease
mortality.
• Flaxseed supplement (2 tbsp oil qd) may be effective but has no effect on
LDL and induces only minor reduction in trigs.
• Garlic extract: no significant long-term change in lipids
• Guggul or guggulipid: overwhelming evidence showed it to be
ineffective for lipids • CoQ10: no solid evidence whether it helps limit
muscle pain with statins, but it is not likely to harm • With high LDL
total cholesterol levels, the patient may try 1 to 2 caps cod liver oil qd, 4 g
of fresh bulb garlic, or 4 to 12 mg of allicin (Kwai) qd.

Hypertension

I. Definition

A. Diagnosis is made after three or more elevated readings at different

times; at each visit, check the BP at least twice with the patient sitting
for at least 5 minutes. Average the readings and classify by the highest
reading—systolic or diastolic (Table 8-12).

269
 B. For pediatric HTN, see Index.
C. Severe HTN: ≥180/≥120 mmHg
1. May present with acute, life-threatening complications (hypertensive
emergencies); emergent transfer to ED
a) encephalopathy
b) retinal hemorrhage or papilledema or severe H/A with vision changes
c) acute renal failure
2. May be asymptomatic other than possible H/A, with no signs of end-
organ damage (hypertensive urgencies); often secondary to
nonadherence with therapy or to recent increased salt intake 3.
Treatment goal: decrease BP to <160/100 mmHg over several hours to
days; there is no proven benefit from rapid reduction in an
asymptomatic patient
a) have the patient rest in a quiet room and recheck BP
b) with previously treated HTN, is the patient taking the medications?
(1) increase dose of existing med or add second one
(2) restart meds if the patient has been nonadherent
(3) with suspicion of HTN due to high salt intake, add diuretics and
reinforce sodium restriction
c) in previously untreated HTN
(1) consider transfer to ED (if the patient is symptomatic with other than
mild H/A) or administer clonidine 0.2 mg or captopril 6.25 to 12.5 mg;
observe the patient up to a few hours to be sure that BP goes down by
at least 20 to 30 mmHg (2) prescribe longer-acting medication (i.e.,
calcium channel blocker, ACE, or ARB)
d) follow-up within a few days
II. Initial workup

A. Specific history questions

1. Past medical history
a) cardiovascular, cerebrovascular, or renal disease
b) DM

270
 c) history of HTN (what level, any treatment, and results); especially
with BP >180/120 mmHg, what has been patient’s adherence with
medical therapy?
d) sleep apnea
e) current medications (prescription and OTC)
f) cardiovascular risk factors (e.g., smoking, hyperlipidemia,
microalbuminuria, or eGFR <60 ml/min) (see Chapter 12, Chronic
Kidney Disease)
2. Social factors: sexual function, exercise, work schedules, how to pay
for medications, and alcohol intake 3. Family history: HTN, CVA,
CHD, HF, renal disease (including polycystic kidneys), DM,
pheochromocytoma, cardiomyopathy, and sudden death
B. Physical examination: main goals are to evaluate for signs of end-
organ damage and evidence of an identifiable cause of HTN
1. General appearance, including calculation of body mass index (BMI)
2. Fundoscopic examination
3. Neck: thyroid and presence/absence of JVD or bruits
4. Cardiovascular: heart sounds (including S4), PMI, breath sounds,
edema, and peripheral pulses 5. Abdomen: liver, presence/absence of
bruits in the abdomen and femoral areas, and presence/absence of
abnormal aortic pulsation 6. Neurological: cranial nerves, DTRs, and
sensory changes
C. Diagnostic tests
1. Laboratory values: CBC, complete metabolic profile, lipid profile, TSH
and free T4, and UA (including albumin/creatinine ratio to estimate
proteinuria—see Chapter 16, Chronic Complications, II, B) 2. ECG
III. Secondary HTN workup

A. Evaluate for secondary HTN with the following:

1. Renal artery stenosis/renovascular disease
a) very severe HTN that is resistant to therapy
b) recurrent episodes of flash pulmonary edema
c) acute rise in BP over previously stable levels

271
 d) onset before the age of 30 years or stage II HTN after the age of 55
years e) acute rise (over 30%) in serum creatinine after administration
of ACE or ARB
2. Primary aldosteronism
a) muscle weakness
b) polyuria
3. Pheochromocytoma
a) resistant or paroxysmal HTN
b) triad of palpitations, H/A, and diaphoresis
c) HTN and new-onset DM
d) onset of HTN before 20 years of age
4. Thyroid disorder
a) fatigue and/or anxiety
b) weight gain or loss
5. Renal injury
a) flank pain
b) trauma
6. Obstructive sleep apnea
a) daytime somnolence
b) fatigue
c) loud snoring
B. Test for renal artery stenosis (i.e., renal angiography or renal artery
duplex Doppler U/S or renal CT angiography) only if:
1. There is a moderate or high risk of having renal artery stenosis and 2.
A corrective procedure would be done if a clinically significant
renovascular disease is found
IV. Treatment of HTN (according to JNC 8 [2014])

A. Goals
1. ≤140/90 mmHg: if the patient is <60 years of age or the patient is >18
years of age and has CKD and/or DM; in younger patients without

272
 comorbidities, elevated DBP is a stronger risk factor than SBP
2. ≤150/90 mmHg: if the patient is >60 years of age (if SBP is <140 mmHg
on current treatment, no changes needed); SBP is more important than
DBP as a risk factor 3. Heart failure: optimal BP not defined; consult a
cardiologist for recommendations
B. For emergency treatment of HTN in office (BP ≥180/≥120 mmHg)
1. Transfer to ED if the patient is symptomatic with anything other than
mild H/A 2. Consider captopril 6.25 to 25 mg once or clonidine 0.1 to
0.2 mg initially and then 0.1 mg qh to a maximum of 0.7 mg; use with
caution if the patient is tachycardic or has cardiac decompensation 3.
Start routine medication (e.g., calcium channel blocker, ACE, or ARB)
and recheck q2-3d until BP stabilizes
C. With “white coat” HTN, if BP is not normal in office after 3 to 6
months of observation, treat according to office BP readings despite
readings elsewhere, especially with other risk factors (e.g.,
hyperlipidemia or obesity) D. Patients with prehypertension are twice
as likely to develop HTN as those with normal BP; strongly encourage
lifestyle modifications for those patients E. Initiate lifestyle changes
(start with pre-HTN or stage 1 HTN)
1. Weight reduction if overweight; aim for 5% to 10% body weight
increments 2. Diet: see Table 8-13 for DASH Diet 3. Exercise: regular
physical activity
a) try a 30-minute walk at a rate of 2 to 3 mph 5 times weekly (or an
equivalent exercise) b) overall increase in physical activity (i.e., 10,000
steps); monitor with pedometer
4. Smoking cessation
5. Alcohol: 3 oz of whiskey, 10 oz of wine, or 24 oz of beer daily; women
and thin patients should consume half of these amounts 6. Sodium
restriction <2.4 g qd
F. If lifestyle changes are unsuccessful or with HTN >stage 1 or an
additional risk factor (e.g., DM or CHD), start medication first (or at
least simultaneously) G. There is no uniform agreement as to which
antihypertensive med should be given for initial therapy (see Table 8-
14 for suggestions); recommended options are as follows:
1. Nonblack patient: thiazide diuretic (especially chlorthalidone), ACE or

273
 ARB, or long-acting calcium channel blocker (CCB) (most often a
dihydropyridine) 2. Black patient without kidney disease: CCB,
thiazide diuretic (especially chlorthalidone) 3. Any patient with kidney
disease: ACE or ARB; an exception: patient aged >75 years with
impaired renal function should receive CCB or thiazide diuretic
instead 4. Except for additional indications (e.g., rate control with atrial
fib), the amount of BP reduction is more important than the choice of
medication; see Table 8-15 for Antihypertensive Medications and
Dosages and Table 8-16 for Cautions and Contraindications
H. If the BP goal is not reached within a month of starting treatment:
1. Increase drug dose or
2. Substitute another drug (“sequential monotherapy”) or
3. Add a second agent
a) thiazide, if not already on one, is a good choice
b) if the patient is on a beta-blocker (BB), use thiazide or dihydropyridine
calcium channel blocker (CCB); ACE or ARB may be less effective
because BB decreases renin secretion and thus angiotensin II formation
c) caution with using BB in combination with nondihydropyridine
CCB (e.g., verapamil or diltiazem) because of an increased risk of
bradycardia or AV block
4. Better response is shown with less side effects, if medication is
changed, or if additional med is added after one-step dose increase
(instead of the maximum dose before adding another med)
I. If the BP goal is still not met after 1 to 2 months, consider triple therapy
with ACE or ARB, CCB, and thiazide diuetic before using any other
class of antihypertensive med. Most patients will require two or more
antihypertensive agents.
J. Resistant HTN is diagnosed when the BP goal is not met despite the
patient adhering to full doses of a three-drug regimen that includes a
diuretic; consultation with a cardiologist should be considered.
Table 8-12
Classification of Hypertension

Classification Systolic Reading Diastolic Reading Follow-up

Normal <120 mmHg <80 mmHg
Prehypertension 120-139 mmHg 80-89 mmHg Recheck in 1 yr

274
 Stage I HTN 140-159 mmHg 90-99 mmHg Recheck in 2 mos
Stage II HTN ≥160 mmHg ≥100 mmHg Treat and recheck in 1
mo
Diagnosis in >30 mmHg above base or >15 mmHg above base or Refer to a high-risk
pregnancy >140 mmHg >90 mmHg obstetrician
Data from the Eighth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure (JNC8) (2013). National High Blood Pressure Education Program; National Heart, Lung, and Blood Institute; National Institutes
of Health.

Table 8-13
The DASH Diet*

Food Group
& Daily 1 Serving Equals Examples
Servings
Grains and 1 slice bread Whole-grain breads, pita, English muffin, bagel, grits,
grain products ½ cup dry or cooked oatmeal
7-8 servings cereal, pasta, or
cooked rice
Vegetables 1 cup raw leafy Tomatoes, potatoes, carrots, peas, squash, broccoli, turnip
4-5 servings vegetables greens, kale, collards, spinach, artichokes, sweet potatoes
½ cup cooked
vegetables
6 oz vegetable juice
Fruits 8 oz fruit juice 1 Apricots, bananas, dates, grapes, oranges, grapefruit,
4-5 servings medium fruit mangoes, melons, peaches, pineapples, prunes, raisins,
¼ cup dried fruit strawberries, tangerines
½ cup fresh, frozen,
or canned fruit
Low-fat and 8 oz milk Skim or 1% milk, low-fat buttermilk, nonfat or low-fat
nonfat dairy 1 cup yogurt yogurt, part-skim mozzarella cheese, nonfat cheese
products 1½ oz cheese
2-3 servings
Meat, poultry, 3 oz cooked meats, Lean cuts with visible fat and skin removed; broiled,
fish poultry, or fish roasted, or boiled
2 or fewer
servings
Nuts and ¾ oz or ⅙ cup nuts Almonds, filberts, mixed nuts, peanuts, walnuts, pecans,
legumes 1 tbsp seeds sunflower seeds, kidney beans, lentils
1 serving ½ cup cooked
legumes
*TheDietary Approach to Stop Hypertension (DASH) diet is low in fat and cholesterol; high in fiber, potassium, calcium, and magnesium;
and moderately high in protein. It provides approximately 2000 kcal a day.

Table 8-14
Suggested Initial Antihypertensive Agents*

Patient Profile Suggested Agent* Agents to Avoid

Angina Nondihydropyridine CCB

275
 Beta-blocker

Asthma, COPD CCB Beta-blocker (not cardioselective)

Central alpha agonist

Atrial fibrillation Nondihydropyridine CCB

Beta-blocker

BPH Alpha-blocker†

HF, diastolic CCB (especially verapamil) Alpha-blocker

ACE or ARB Beta-blocker with ISA‡
Dihydropyridine CCB
Direct vasodilator
Diuretic

HF, systolic ACE or ARB Most CCB and alpha-beta blockers

Beta-blocker (specifically carvedilol,
metoprolol)
Diuretics

Depression Beta-blockers
Central alpha agonist

DM, type 1 ACE or ARB Beta-blocker with ISA‡

Thiazide diuretic (especially Alpha-blocker
chlorthalidone)
Central alpha agonist

DM, type 2 ACE or ARB Diuretic at high dose

CCB Beta-blocker (except carvedilol)

Elderly Diuretic Alpha-blocker (use cautiously because of

CCB postural hypotension)

Ischemic heart Beta-blocker without ISA‡ Beta-blocker with ISA‡

CCB Vasodilator

Isolated systolic HTN Diuretic CCB

Left ventricular hypertrophy ACE or ARB Beta-blocker with ISA‡

CCB Direct vasodilator

Peripheral vascular disease CCB Alpha-blocker

Renal insufficiency Loop diuretics usually needed with Beta-blocker

advanced renal disease
ACE or ARB (depends on the cause)

Tachycardia CCB (especially verapamil or diltiazem)

Young or with Beta-blocker

hyperdynamic circulation ACE or ARB

*Also see Table 8-15 for dosing guidelines and Table 8-16 for cautions.
†Not as a primary agent but may be useful as an add-on agent, especially in elderly men with symptomatic prostatism.

276
‡Intrinsic
sympathomimetic activity (i.e., blocks beta1 receptors while mildly stimulating beta2 receptors).

Table 8-15
Antihypertensive Medication and Dosages

Maintenance
Medication Initial Dose
Maximum
ACE Inhibitors (ACE)
Benazepril (Lotensin)* 10 mg qd 80 mg qd

Captopril (Capoten)* 25 mg bid-tid 450 mg qd

Enalapril (Vasotec)* 2.5 mg qd (with diuretics) 40 mg qd

5 mg qd (without diuretics)

Fosinopril (Monopril)* 10 mg qd 80 mg qd

Lisinopril (Zestril, Prinivil)* 10 mg qd 40 mg qd

Quinapril (Accupril)* 10 mg qd 80 mg qd

Ramipril (Altace) 2.5 mg qd (may be opened and mixed with 20 mg qd

applesauce, water, or apple juice)

Moexipril (Univasc)* 7.5 mg qd 1 h ac 30 mg qd

Trandolapril (Mavik) 1 mg qd 8 mg qd

Perindopril (Aceon) 4 mg qd 8 mg qd

Angiotensin II Receptor Blocker (ARB)

Azilsartan (Endarbi)* 40 mg qd 80 mg qd

Candesartan (Atacand)* 16 mg qd (lower dose if volume depleted or on 32 mg qd in 1-2

other antihypertensive agents) divided doses

Irbesartan (Avapro)* 150 mg qd 300 mg qd

Losartan (Cozaar)* 50 mg qd (25 mg with volume depletion or hepatic 50 mg bid or 100 mg

impairment) qd

Olmesartan (Benicar)* 20 mg qd 40 mg qd

Telmisartan (Micardis)* 40 mg qd 80 mg qd

Valsartan (Diovan)* 80 mg qd 320 mg qd

Eprosartan mesylate (Teveten)* 600 mg qd 800 mg qd, in 1-2

divided doses
†
Alpha Adrenergic Blocker (Peripheral)
Prazosin (Minipress) 1 mg bid-tid 15 mg qd

Terazosin (Hytrin) 1 mg hs 20 mg qd

Doxazosin mesylate (Cardura) 1 mg qd 16 mg qd

Alpha Agonist (Central)

277
Clonidine (Catapres) 0.1 mg bid 2.4 mg qd

Methyldopa (Aldomet)* 250 mg bid-tid 3000 mg qd

Alpha-Beta Blocker

Carvedilol (Coreg) 6.25 mg qd or bid 50 mg qd

Labetalol HCl (Normodyne, Trandate) 100 mg bid 1200 mg in bid dose

Beta-Blocker
Metoprolol tartrate (Lopressor)*, metoprolol 50-100 mg qd 450 mg qd
succinate (Toprol XL)

Nadolol (Corgard) 40 mg qd 320 mg qd

Propranolol HCl (Inderal)* 40 mg bid 640 mg qd total

(Inderal LA) 80 mg qd 640 mg qd

Bisoprolol fumarate* 5 mg qd 20 mg qd
‡
Beta-Blocker with ISA
Acebutolol (Sectral) 400 mg qd 1200 mg qd

Pindolol (Visken) 5 mg bid 60 mg qd

Calcium Channel Blockers (Nondihydropyridines)

Diltiazem: 60-120 mg bid 360 mg qd
• Cardizem SR 120-240 mg qd 360 mg qd
• Cardizem CD, Tiazac 180-240 mg qd 540 mg qd
• Cardizem LA

Verapamil (Calan SR, Isoptin SR, Verelan) 120-240 mg qd 480 mg qd

Calcium Channel Blockers (Dihydropyridines)

Amlodipine (Norvasc) 2.5-5 mg qd 10 mg qd

Felodipine (Plendil) 5 mg qd 10 mg qd

Isradipine (DynaCirc) 2.5 mg bid 20 mg qd

Nicardipine (Cardene SR) 30 mg bid 120 mg qd

Nifedipine 30-60 mg qd 120 mg qd

• Procardia XL 30-60 mg qd 90 mg qd
• Adalat CC

Nisoldipine (Sular) 20 mg qd 60 mg qd

Direct Renin Inhibitor

Aliskiren (Tekturna)* 150 mg qd 300 mg qd

Direct Vasodilator
Hydralazine (Apresoline) 10 mg qid 300 mg qd

Loop Diuretics
Bumetanide (Bumex) 0.5-2 mg qd 10 mg qd

278
 Furosemide (Lasix) 40 mg bid 80 mg qd

Torsemide (Demadex) 5 mg qd 10 mg qd

Potassium-Sparing Diuretics
Amiloride 5 mg qd 10 mg qd

Eplerenone (Inspra) 50 mg qd 50 mg bid

Spironolactone (Aldactone) 25 mg qd 50 mg qd

Triamterene (Dyrenium) 50 mg qd 300 mg qd

Thiazide Diuretics
Chlorothiazide (Diuril) 500-1000 mg qd 2000 mg qd

Chlorthalidone 12.5 mg qd 100 mg qd

Hydrochlorothiazide (Microzide) 6.25-25 mg qd 50 mg qd

Indapamide (Lozol) 1.25 mg qd 5 mg qd

Metolazone (Zaroxolyn) 2.5-5 mg qd 5 mg qd

*Also
comes in combination with a diuretic.
†Give
the initial dose at bedtime to decrease syncopal episodes; not a first-line BP medication.
‡Intrinsic
sympathomimetic agent (i.e., blocks beta1 receptors while mildly stimulating beta2 receptors).
See Table 8-16 for Cautions and Contraindications. Combination agents are not included in this chart.

Table 8-16
Cautions and Contraindications for Antihypertensive Agents

Medication Precautions Contraindications

ACE inhibitors Monitor serum potassium, BUN, and creatinine at Hypertrophic cardiomyopathy
(ACE) baseline and 2-3 wks after dose increases; stop if Bilateral renal artery stenosis or
creatinine increases by ≥1 mg/dl Use cautiously in stenosis of a solitary kidney
women of child-bearing age and not on contraception
Pregnancy (consider urine or serum
Discontinue therapy if the patient develops angioedema
HCG before use)
(swelling of hands, face, or tongue), sore throat, or fever
(of undetermined origin)

Angiotensin II Monitor serum potassium, BUN, and creatinine at Pregnancy (consider urine or serum
receptor blockers baseline HCG before use)
(ARB) Use cautiously if the patient is volume depleted Renal artery stenosis (as above)
Use cautiously in women of child-bearing age and not on CKD (eGFR ≤30 ml/min)
contraception

Alpha-blockers May have postural BP changes (especially with the first Hypertrophic cardiomyopathy
(peripheral) dose or after a missed dose) Elderly patients
Cautious use with hepatic impairment (doxazocin)

Alpha agonists May have postural BP changes Active hepatic disease and in elderly
(central) Preexisting bradycardia patients (methyldopa)

Concomitant depression
Taper slowly because of rebound HTN

279
 Severe coronary insufficiency
Chronic renal impairment

Alpha-beta blockers Monitor heart rate Asthma

May have postural BP changes Overt HF (labetolol)
Type 1 or 2 DM Severe bradycardia
COPD AV block greater than first degree
Hepatic impairment (mild to moderate) Severe hepatic impairment
PVD/Raynaud phenomenon
Pregnancy
Children

Beta-blockers Monitor the heart rate for bradycardia Type 1 DM

Peripheral vascular disease (PVD) Asthma/COPD
Type 2 DM or pre-DM (except carvedilol and nebivolol) Severe HF
Hyperlipidemia Sick sinus syndrome or AV blocks
May be less effective in African Americans Severe PVD
Taper slowly because of rebound HTN (possible MI or Raynaud phenomenon
sudden death with sudden stopping)
Pregnancy (atenolol)

Beta-blockers with May accelerate ischemia in CAD

ISA* Taper slowly because of rebound HTN (possible MI or
sudden death with sudden stopping) Asthma/COPD

Calcium channel Monitor heart rate for bradycardia Bradycardia

blockers (CCB): May aggravate CHD and HF AV blocks
nondihydropyridines
Constipation (especially verapamil) Severe left ventricular systolic
dysfunction

Calcium channel May cause lightheadedness, H/A, peripheral edema

blockers (CCB):
dihydropyridines

Direct renin inhibitor eGFR <30 ml/min or creatinine >2

mg/dl (males) or >1.7 mg/dl (females)

Direct vasodilators May precipitate angina in CAD Mitral valve rheumatic heart disease
Pulmonary HTN
Severe renal impairment
Concomitant treatment with a diuretic or beta-blocker
may be indicated

Diuretics: loop Monitor electrolyte panel plus Mg++ Preeclampsia

Monitor weight Hepatic coma (bumetanide)
May develop tolerance; using staggered dosing may Hypertrophic cardiomyopathy
decrease tolerance (relative contraindication)
Ototoxicity may occur with high doses of furosemide Sulfa allergy
Cirrhosis, ascites
Hypokalemia (see Table 8-17 for treatment)

Diuretics: potassium Monitor electrolytes Preexisting hyperkalemia

sparing DM Acute renal insufficiency: creatinine

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 Concomitant use of NSAIDs or ACE >2.5 mg/dl (males) or >2 mg/dl
Use cautiously, if at all, with creatinine >1.5 mg/dl (females) Severe hepatic disease
(triamterene: no; eplerenone: caution)
Hepatic impairment (spironolactone)

Diuretics: thiazide
Monitor electrolyte panel plus Mg++ and Ca++ before Sulfa allergy
starting and recheck K+ after 3 wks on med Serum creatinine >2.5 mg/dl
Hyperlipidemia (moderate-to-high cholesterol) (ineffective in severe renal disease)
Type 2 DM or pre-DM
Hypertrophic cardiomyopathy
Hypokalemia (see Table 8-17 for treatment) (relative contraindication)
Cirrhosis Preeclampsia
Systemic lupus erythematosis (SLE) Poorly controlled gout

*Intrinsic
sympathomimetic activity (i.e., blocks beta1 receptors while mildly stimulating beta2 receptors).
See Table 8-15 for dosing recommendations.

P r a c t i c e Pe a r l s f o r H y p e r t e n s i o n

• Follow up q1-2mo, depending on the status, until the BP goal is reached. Once stable,
follow-up visits can be at 3-to 6-month intervals. In patients aged >50 years, SBP is a more
important CVD risk factor than DBP.
• Do not give an ACE and ARB simultaneously.
• Recheck basic chemistry profile 2 to 3 weeks after starting an ACE; if creat has increased,
recheck again in 2 to 3 weeks. If creat level has increased further, stop the ACE.
• When the patient is on more than one antihypertensive medication, taking one nondiuretic
med at hs may improve BP control.
• With difficulty controlling BP, ask about herbs (e.g., ginseng can decrease the efficacy of
many antihypertensive agents).
• NSAIDs may interfere with the effects of ACE inhibitors, beta-blockers, and diuretics.
• Treat with decongestants cautiously; pseudoephedrine has the lowest cardiovascular risk
profile.
• Thiazides are more effective than loop diuretics in HTN, except when serum creatinine is
>2.5 mg/dl.
• Potential side effects

• Coughing could be due to ACE; if bronchospasms occur, consider the

effect of beta-blockers; if the patient currently smokes, choose a
cardioselective beta-blocker.
• Sexual or erectile dysfunction may occur with alpha-blockers, beta-
blockers, and central alpha agonists.

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 • Edema with amlodipine is not fluid related, so diuretics do not help;
try decreasing the dose, adding an ACE/ARB, or changing to a
different medication.
• Diuretics can elevate serum cholesterol and triglyceride levels and
decrease HDL levels in diabetics.
• Olmesartan (Benicar) has been associated with spruelike illness (i.e.,
severe, chronic diarrhea, significant weight loss); the condition resolves
when the med is stopped.
• Potassium supplementation may be needed when taking diuretics (see Table 8-17).

Metabolic syndrome

I. Description: This condition is characterized by insulin resistance and prothrombotic and

proinflammatory states; it markedly increases the risk for CHD
II. Diagnosis: metabolic syndrome is diagnosed when any three or more of the following
symptoms are present:

A. Abdominal obesity (waist circumference)

1. Men: >40 inches (102 cm)
2. Women: >35 inches (88 cm)
B. Triglycerides: ≥150 mg/dl
C. HDL cholesterol level
1. Men: <40 mg/dl
2. Women: <50 mg/dl
D. BP: ≥130/85 mmHg or on medication for hypertension
E. FBG level: ≥100 mg/dl
III. Management

A. Reduce and/or treat the underlying causes and conditions

B. Encourage dietary changes and, if indicated, weight reduction (in 5%
increments) C. Encourage increased physical activity
1. Work up to 30-minute walks 5 times a week (or an equivalent exercise)
2. Increase overall daily movement (i.e., aim for 10,000 steps daily,
monitor with a pedometer)
D. Consider ASA 81 mg/day for patients with CHD (see Practice Pearls

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 for Angina)
Table 8-17
Potassium Supplementation

Dosing
Prevention 16-24 mEq qd
To correct depletion 40-100 mEq qd
Suggested Products
8 mEq Klor-Con 8 or Slow-K
10 mEq K-Dur 10, K-Tab, Kaon 10, Klor-Con 10
20 mEq K-Dur 20, 15 ml of Kaochlor 10% liquid
25 mEq K-Lyte/Cl effervescent
50 mEq K-Lyte/Cl 50 effervescent

Bacterial endocarditis antibiotic prophylaxis*

I. High risk (always pretreat)

A. Prosthetic heart valve or prosthetic material used for heart valve

repair B. History of endocarditis
C. Unrepaired cyanotic congenital heart disease
D. Repaired congenital heart disease with residual defects at the site of or
adjacent to the site of the prosthetic device E. Heart transplant that
develops problems in a heart valve
II. Negligible risk (do not need to pretreat)

A. Surgically repaired congenital heart defects

B. History of coronary artery bypass graft surgery
C. Calcified aortic stenosis
D. Mitral valve regurgitation and mitral valve prolapse
E. Rheumatic heart disease
F. Bicuspid valve disease
G. Physiological, functional, or innocent murmurs
H. Previous rheumatic fever without valve damage
I. Pacemakers or implanted defibrillators
J. Before an EGD, colonoscopy, or GU procedures
III. See Table 8-18 for Antibiotic Prophylaxis Regimens

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Table 8-18
Antibiotic Prophylaxis Regimens for Bacterial Endocarditis

Patient Status Agent

Regimen
Not allergic to penicillin and able to take Amoxicillin
Adult: 2 g 1 h before procedure
oral medication Child: 50 mg/kg 1 h before
procedure
Not allergic to penicillin but unable to take Ampicillin Adult: 2 g IM or IV within 30 min
oral medication of procedure
Child: 50 mg/kg IM or IV within 30
min of procedure
Allergic to penicillin Clindamycin Adult: 600 mg 1 h before procedure
Azithromycin Child: 20 mg/kg 1 h before
procedure
Adult: 500 mg 1 h before procedure
Child: 15 mg/kg 1 h before
procedure
Allergic to penicillin and unable to take oral Clindamycin Adult: 600 mg IV within 30 min of
medication procedure
Child: 20 mg/kg IV within 30 min of
procedure

*For
dental procedures (NOT including routine dental cleaning) or respiratory tract procedures involving incision or biopsy of the
respiratory tract mucosa.

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CHAPTER 9

285
Peripheral vascular and hematologic
conditions
Chronic peripheral vascular diseases

Peripheral venous disease

I. Deep vein thrombosis (DVT)

A. Description: presence of a thrombus in one of the deep venous

conduits that return blood to the heart; if left untreated, the thrombus
may dislodge and migrate to obstruct arterial supply to the lung,
causing pulmonary embolism
B. Can be found in the upper or lower extremities
C. Potential causes of DVT
1. Increased platelet adhesiveness due to estrogen or antiestrogen
therapy (e.g., OC or tamoxifen)
2. Immobility (e.g., prolonged travel, major surgery with immobility)
causing a 50% decrease in blood flow to the legs, leading to stasis
3. Long bone trauma or crush injury (especially of the femur)
4. Hyperfibrinogenemia during pregnancy and first postpartum month
5. Increased blood viscosity due to high altitude changes
6. Nephritic syndrome, polycythemia vera, cancer
7. Deficiency of endogenous anticoagulants
8. Morbid obesity
9. Varicose veins due to stasis
D. Signs and symptoms
1. Unilateral pain, aching, or cramping in the affected calf or thigh that is
aggravated by muscle activity
2. Swelling in the affected limb, including foot and ankle; usually
unilateral

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 3. Localized tenderness to palpation, which is marked at the site of
occlusion
4. Increased warmth to touch
5. Tender, cordlike vein (uncommon)
6. May see a change in the color of the affected extremity, with pale, red,
or blue discoloration
7. Positive Homan’s sign (accurate <30% of time)
E. Diagnostic testing
1. Doppler U/S
2. Contrast venography (gold standard)
F. Treatment
1. Transfer to ED if PE or extensive DVT is suspected
2. May be treated as an outpatient if no PE
3. Anticoagulant therapy is recommended for 3 to 12 months (first
episode) or for lifetime (recurrent DVT). Selected agents
a) enoxaparin (Lovenox) 1 mg/kg SQ q12h for 5 to 7 days, and begin
warfarin within 72 hours of diagnosis
b) fondaparinux (Arixtra) SQ (dose dependent on weight) daily for 5 to 7
days, overlapping warfarin with a target INR of 2 to 3
c) rivaroxaban (Xarelto) 15 mg bid PO for 21 days, then 20 mg qd for 6
months (or lifetime depending on the circumstances)
d) warfarin therapy (see Ambulatory Warfarin Therapy in this Chapter)
4. Follow-up care for routine monitoring (INR as scheduled, CBC
monthly if bleeding tendency)
5. Stop OC/HRT
6. Avoid crossing legs, prolonged sitting/standing, or massaging of
extremity
7. Stop smoking
8. Wear antiembolic stockings to decrease recurrent thrombosis and post-
thrombotic syndrome
II. Superficial thrombophlebitis

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 A. Description: a thrombus in a surface vein causing inflammation and
phlebitis; usually occurs in the lower extremities, but can occur in any
region affected by medical intervention
B. Signs and symptoms
1. Presents as redness along the course of a vein, with swelling and
warmth
2. May be able to see inflamed portions of the vein
3. Pain on palpation of the reddened area
C. Diagnostic testing: Doppler U/S
D. Treatment
1. Hot, moist packs
2. Elevation and relaxation of the extremity
3. Preferably long-leg graduated compression stockings, usually with a
pressure of 30 to 40 mmHg
4. NSAIDs
5. Consider anticoagulant therapy for a short period of time, such as
enoxaparin 40 mg qd for 4 weeks or warfarin for 3 months with a
target INR range of 2 to 3
6. Smoking cessation, weight loss, and increased mobility
7. Follow-up in office in 24 to 48 hours
III. Chronic venous insufficiency (CVI)

A. Description: a slow progressive disorder in the superficial or deep

venous system in legs; impedes return flow to the heart, causing
edema, skin changes, and ulceration
B. Risk factors
1. Elderly
2. Previous DVT (<30%)
3. Varicose veins
4. History of prolonged standing, sitting, or decreased mobility
5. Obesity

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C. Signs and symptoms
1. Edema that progresses from distal to proximal; may be unilateral or
bilateral
2. Dullness, aching, tiredness, or heaviness in legs
3. Hemosiderin (bronzing) staining of the skin
4. Scaly skin with cutaneous atrophy
5. Tingling, itching, “hot legs”
6. Pain in legs that improves with walking and with elevating legs at rest
7. Pain worsens with dependent position
8. Stasis dermatitis leading to ulceration
D. Diagnostic testing
1. ABI (see Calculation of ABI in this chapter): considered gold standard
2. Doppler U/S
3. Magnetic resonance venography (MRV)
E. Treatment
1. Weight management
2. Decrease edema
3. Four to six 30-minute rest periods during the day, with feet elevated
above thighs
4. Gradually increase exercise with walking, bicycling, and swimming
5. Graduated compression stockings (see Compression Stocking Therapy
in this chapter) to improve circulation through support to veins
a) TED hose or Jobst hose
b) Unna boot (see Unna Boot Application in this chapter)
6. Meticulous skin care and monitoring for ulcerations/wounds
7. Aggressive wound care, with referral to a wound care specialist at the
earliest opportunity
8. Pharmacotherapy
a) ASA 81 mg daily

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 b) pentoxifylline 400 mg tid or cilostazol 50 to 100 mg bid may aid in
venous ulcer wound healing
c) horse chestnut seed extract 300 mg bid may reduce edema and leg
pain in mild CVI
IV. Stasis dermatitis

A. Description: leakage of fluid/blood cells into the skin and tissues of

lower legs, causing itching
1. Secondary to Chronic Venous Insufficiency
2. Caused by consistent elevation in venous pressure from obstruction,
valve dysfunction, decreased “venous pump” effectiveness (muscle
contraction)
B. Signs and symptoms
1. Thin, erythematous skin with reddish-brown pigmentation patches
over the lower legs initially changing to a violaceous color with scales,
vesicles, and crusts
2. Bumpy or cobblestone appearance
3. Itching and pain related to swelling
4. Lichenification and thickening of the skin due to scratching
5. Skin ulcers more common on medial aspects of the ankles
C. Diagnostic testing
1. Doppler U/S if DVT suspected
2. ABI (see Calculation of ABI in this chapter)
3. CBC and comprehensive chemistry panel
D. Treatment
1. Avoid OTC topical antibiotics with neomycin (can cause dermatitis);
can use bacitracin or bactroban
2. Frequent elevation of feet above thigh level
3. Drying solutions and topical local anesthetics may help alleviate
discomfort
4. Use topical steroids early in treatment
5. Oral antibiotics for cellulitis for 10 days

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 a) cephalexin 250 to 500 mg tid
b) TMP/SMX DS bid
c) ciprofloxacin 250 to 500 mg bid
6. Graduated compression stocking therapy (see Compression Stocking
Therapy in this chapter): apply before getting out of bed in the
morning
V. Varicose veins

A. Description: occurs when valve damage permits backflow of blood,

causing engorgement of veins, primarily in the greater and lesser
saphenous system
B. May lead to Chronic Venous Insufficiency with an increased risk of
DVT (usually one leg affected more than the other)
C. Signs and symptoms
1. Tortuous, dilated superficial vessels, predominantly in the lower legs
2. Heaviness, fatigue, and aching in legs (relieved with elevation of legs)
3. Affected limb is edematous
4. Patient will often complain of night cramps
D. Diagnostics: Doppler U/S and/or venogram
E. Treatment
1. Periodically elevate feet above thighs
2. Avoid prolonged standing/sitting and constrictive clothing at the waist
and groin
3. For best results, apply any type of support stockings before getting out
of bed
4. Avoid OC/HRT
F. Refer for surgical consultation

Peripheral arterial disease

I. Acute arterial occlusion (acute limb ischemia)

A. Description: acute arterial occlusion usually caused by a thrombus

secondary to atherosclerosis or other occlusive diseases; other

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 contributing factors may be arterial injury after surgery, DIC, sepsis,
hypercoagulability disorders
B. Signs and symptoms
1. Decreased PT pulse demonstrates increased sensitivity for PAD
2. Loss of peripheral pulses distal to occlusion
3. Bruit is common if arterial plaque is the source of embolus
4. Six Ps indicative of emergent occlusion
Pain
Pulselessness
Pallor
Paralysis
Paresthesia
Poikilothermia
C. Treatment is urgent/emergency transfer to ED or a vascular surgeon
II. Chronic arterial occlusive disease

A. Description: arterial stenosis causing altered blood flow

1. Normally with exercise, blood flow increases to allow muscle function;
however, in occlusive disease, claudication occurs because the
metabolic demands of the muscle exceed the actual blood flow
2. Occurs commonly in the terminal aorta, iliac, superficial femoral, and
popliteal arteries. This begins as stenosing lesions that progressively
narrow to complete obstruction.
3. Is related to smoking, atherosclerosis, HTN (poorly controlled), lack of
exercise, obesity, hyperlipidemia, and DM
4. Diabetics are at the highest risk of loss of an extremity because of
occlusion of larger and smaller arteries
B. Signs and symptoms
1. Gradual onset unless acute thrombosis occurs
2. Intermittent claudication: reproducible cramping pain or ache in legs
that occurs with exercise and is relieved with rest (within 2 to 5
minutes of rest); severity is graded according to exercise

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a) mild: can walk two blocks with little interference and can perform
ADLs
b) moderate: pain with walking one or two blocks; some interference
with ADLs
c) severe: pain with walking less than half to one block; significant
interference with ADLs
3. Fatigue/weakness in legs while walking
4. Possible location of occlusion
a) pain in calves: usually from occlusion in the femoral, popliteal, or
tibial arteries
b) pain in buttocks, hip, or thighs: usually from occlusion in the aorta or
iliac arteries
5. Pain usually progresses to night pain
6. Pain and pallor in feet worsened by elevation; pain and red color
relieved with dangling; patient usually sleeps with feet dangling to
decrease pain
7. Lack of hair on the affected extremity; possible skin breakdown with
small non-inflamed ulcers
8. Thickened nails; cold hands and feet
9. May have diminished pulses and/or bruits in aortic/femerol artery
10. Associated with xanthelasma of eyelids
C. Diagnostics
1. ABI (see Calculation of ABI in this chapter and Table 9-1)
2. Doppler U/S
3. Arteriogram
4. Check pedal pulses at rest and with exercise; check pulses for bruits
from abdominal aorta to feet using portable Doppler
5. CBC, chemistry panel
6. Check blood pressure in both arms and legs
D. Treatment

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 1. Smoking cessation (most important factor)
2. Control hyperlipidemia
3. Exercise program to control collateral circulation (see Exercise
Program for PAD in this chapter)
4. Control HTN, DM
5. Close monitoring of skin for ulcer prevention or early treatment
6. Antiplatelet agents
a) ASA 81 to 325 mg daily
b) clopidogrel 75 mg daily to decrease the risk of MI or CVA
c) pentoxifylline 400 mg tid or cilostazol 100 mg 1 to 2 times daily may
help alleviate pain and increase walking distance
7. Other drug therapies
a) ACE inhibitor qd
b) statins for control of lipids (see Hyperlipidemia, V, C in Chapter 8)
E. Refer to a vascular surgeon for follow-up
III. Raynaud’s phenomenon

A. Description: recurrent vasospasm of fingers and toes in response to

stress or cold exposure
1. No association with any other disease processes
2. Symmetrical bilateral involvement, absence of necrosis
3. Normal laboratory findings and negative ANA
4. Secondary Raynaud’s phenomenon is usually associated with an
autoimmune disease and progresses with tissue damage
B. Signs and symptoms
1. Numbness and pain in the affected area(s)
2. Affected areas show at least two different color changes (red, blue, or
white), usually starting with white and progressing to blue before red
a) these changes have a sharp border demarcation between affected and
unaffected areas
b) changes should be reversible

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 C. Diagnostics
1. CBC (may show polycythemia)
2. Chemistry panel (check for possible renal or hepatic involvement,
early/late diabetes); TSH
3. ANA/RA and antiphospholipid antibodies; catecholamines may also
be indicated
D. Treatment
1. Avoidance of causative factors
2. Use gloves and warm clothing
3. Medications (to help control symptoms)
a) calcium channel blockers, such as nifedipine at the lowest dose (can
use nicardipine, amlodipine, or diltiazem if side effects occur from
nifedipine)
b) ARBs such as losartan 50 mg daily
c) SSRI such as fluoxetine
d) topical nitroglycerin (1% to 2%) applied to severely affected digits
4. Medications that may worsen the condition
a) beta-blockers, clonidine, caffeine
b) imipramine
c) Sudafed, weight loss supplements, amphetamines
d) OC and ergots
e) alcohol
Table 9-1
ABI Interpretation

ABI Disease Severity

>1.30 Noncompressible, calcified vessels; poor indicator of disease status
0.91-1.3 Normal (no disease)
<0.9* Diagnostic of mild-to-moderate occlusive arterial disease:
0.4-0.9: Borderline disease; claudication symptoms are usually present
<0.40: Severe occlusive disease; ischemia and rest pain common
*Refer to a vascular surgeon.

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Calculation of ankle-brachial index (ABI)

I. Definition: ABI is a diagnostic measure of lower extremity arterial ischemia and should be used
to establish lower extremity PAD in people with exertional leg symptoms, nonhealing ulcers,
and age >65 years or >50 years with smoking or DM
II. Procedure: use a handheld Doppler transducer and place over either the DP or PT artery. The
BP cuff is inflated at the ankle; systolic pressure is recorded when the signal reappears as the cuff
deflates. Brachial systolic pressure is recorded in a similar manner.
III. Calculation: ABI is the ankle pressure divided by the brachial pressure
IV. Interpretation: normal ankle systolic pressure exceeds arm systolic pressure. Ankle pressure
does not begin to change until the artery diameter is reduced by at least 50%. ABI normally does
not fall after exercise. ABI is normal at rest and becomes abnormal with exercise because of
stenosis. Noncompressible arteries can be found in DM and CKD and lead to falsely elevated
readings. See Table 9-1 for ABI Values.

Exercise program for peripheral arterial disease

I. Exercise therapy allows patients with PAD to walk farther and reduces the severity of
symptoms through development of collateral circulation; most patients increase the distance they
are able to walk without claudication in 6 to 12 months
II. A standard program involves walking daily to the point of claudication (patients need to
understand that pain does not indicate that damage is occurring and that it is not harmful)

A. A treadmill at 2 mph
B. An optional mode of exercise is a stationary bicycle with no resistance,
which is easier for overweight people who require non-weight-bearing
exercise
III. The goal is to exercise 45 to 60 minutes daily with resting periods

A. Instruct patients to stop exercising if claudication occurs and resume

exercise as soon as the symptoms resolve
B. Try to increase the exercise duration
IV. As the exercise program continues, the pain should lessen (but may never completely go
away with exercise); the pain scale can be used to document improvement

1 = No pain
2 = Onset of pain
3 = Mild pain
4 = Moderate pain
5 = Severe
V. With peripheral disease, there may also be concomitant coronary artery disease; consider

296
obtaining a stress test before initiating an exercise program

Treatments and interventions for vascular disorders

Compression stocking therapy

I. The amount of compression depends on the severity of the illness; the more severe the
swelling, the higher the pressure. Any compression higher than 20 mmHg should be custom
fitted or applied by a trained individual.

A. For an ABI of 0.6 to 0.8, compression should be about 20 mmHg; for

an ABI of 0.8 to 1.0, compression should be about 30 to 40 mmHg
B. 40 to 60 mmHg stockings (prescription)
1. Can be used if there is no arterial occlusion
2. Used for severe edema and lymphedema or severe venous stasis
C. 30 to 40 mmHg stockings (prescription)
1. Used for DVT
2. Used for severe swelling and lymphedema and for severe varicose
veins
D. 20 to 30 mmHg stockings (prescription)
1. Can be used if there is a possibility of arterial occlusion
2. Used for varicose veins or swelling after surgery
E. 15 to 20 mmHg stockings (OTC)
1. Good for travel
2. Good for assisting circulation without a tight fit, which might benefit
early venous insufficiency
II. Compression stockings

A. Knee-length stockings are preferred, but thigh-high stockings are

appropriate for lymphedema. Length essentially depends on the
wearer’s preference; measure length before ordering.
B. When donning stockings, use some baby powder or cornstarch on the
legs to help the stockings slide up the leg more easily
C. Use rubber gloves to help grip the stockings and with pulling up and
smoothing out the stockings

297
 D. Wash stockings daily and hang up to dry; do not use a dryer
E. Will probably need new stockings q3-6mo because they do stretch
F. Stockings work best if put on before getting out of bed
III. Single-layer compression such as Ace-wrap bandages can be used with cautious application,
because a tourniquet effect is possible if applied too tightly or if the pressure is too high at the
lower levels

A. Usual tension applied is 3 to 4 mmHg

B. Should be applied by a trained person

Unna boot application

I. An Unna boot is a type of gauze impregnated with calamine, zinc oxide, or gels

A. Used to treat CVI ulcers, decrease pain, assist venous return, and
decrease swelling
B. Decreases venous hypertension and weeping of fluids into the lower
leg tissues
C. Increases wound epithelialization and promotes a moist wound bed
for healing
D. Used with ambulatory patients because the benefit is greater if the
person is able to move about and increase circulation
II. Application points

A. Dressing can be left on for 3 to 14 days

B. Do not apply with suspected DVT, HF, cellulitis, or arterial insufficiency
C. Keep the Unna boot dry; may need to use a long plastic bag over the
dressing when showering
III. Application technique

A. Have the patient sit with feet dangling and foot at a 90-degree angle
B. Don gloves; use clean technique during application (no need to use
sterile technique)
C. Check the skin for any ulcers and if present, measure and document
wound description (see Wound Staging and Treatment in this
chapter). Check for pulses (DT, PT) and capillary refill.
D. Clean the skin and apply mineral oil (this will decrease itching); apply

298
 non-adherent dressing to any open wounds
E. Open the wrap and begin at the base of toes. Use a single-layer spiral
wrap without tension; progress toward knee and stop about 1 inch just
below knee. Eliminate creases and do not wrap downward.
F. The spiral wrap should be overlapped by about 50% with each spiral;
cut excess off at knee
G. Flatten the wrap according to the contour of the leg; have the patient
flex the ankle several times to make sure that the dressing is not too
tight
H. Cover the Unna boot with coban (usually about 4 inch in size). Start at
the toes and cover the Unna boot. DO NOT apply this with tension.
Apply with the spiral technique also and if needed, overlap the new
coban but DO NOT wrap downward.
I. Have the patient flex the ankle after coban application
J. Can then apply a stockinette if more covering is required
IV. Educate the patient about possible complications or changes in the current status of the
extremity such as follows:

A. Change in the color of toes

B. Worsened pain after wrap placement
C. Numbness or paresthesia
D. Swelling
E. Increased itching
F. New discharge or foul odor

Ambulatory warfarin anticoagulant therapy

I. Warfarin therapy is still used for anticoagulation after DVT/PE, AF, cardiomyopathy, and other
heart-related injuries or surgeries. It is also used after major joint replacement to decrease the
possibility of postop related DVT/PE.

A. Warfarin is still the most cost-effective product, although it has

numerous dosing difficulties and restrictions
B. Dietary changes (e.g., see Appendix A for foods that are high in
vitamin K) must be made while on warfarin because of interactions
that will either enhance or reduce the effectiveness of warfarin

299
 C. Warfarin has a very narrow and individualized dosing schedule.
Close monitoring of therapeutic levels are required to maintain
anticoagulation and prevent any bleeding risks.
II. Dosing pearls

A. Use single-strength tablets for dosing, which are safer than using
multiples of a dose
B. The majority of people taking warfarin are elderly and have more
trouble calculating doses, cutting pills, filling pill boxes, or
remembering to take the correct dose on the correct day
C. Changes in the dosing schedules are based on the total weekly dose
(TWD) rather than the daily dose. Calculate the total dose for the week
and make changes by 5% to 20% as needed (Table 9-2).
D. Anticoagulation may be seen within 24 hours, with peak effects in 72
to 96 hours; time to steady state is approximately 10 days
III. Check for possible interactions with warfarin when starting any new medication
IV. Grapefruit juice/cranberry juice, any herbal product that starts with a “G” (e.g., green tea,
ginseng, garlic), dong quai, mango, papaya, birch, and foods high in vitamin K (see Appendix A)
can interfere with warfarin
V. A good rule of thumb is as follows: any time a medication is changed or a new medication
added, recheck INR within 3 to 7 days
VI. Contraindications for starting warfarin are all based on the relative risk of thrombosis versus
the risk of bleeding while on warfarin. Some contraindications are as follows:

A. Severe or active bleeding disorder

B. Non-adherence to medication monitoring
C. Pregnancy
D. Allergy or intolerance to warfarin; consider an alternative
anticoagulant if therapeutically indicated
E. Uncontrolled HTN (>180/110 mmHg)
F. High risk of falls
G. Dementia
H. Recent surgery (unless joint replacement) or major risk of thrombosis
VII. Starting warfarin

A. Initially, INR will fluctuate and will need to be checked anywhere

from 2 times a week to once a week until INR starts to normalize.

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 Intervals can be increased when INR reaches therapeutic levels after 2
to 3 checks.
B. Usually start with 5 mg; recheck INR in 3 days and then follow the
chart (see Table 9-2)
C. Review the patient’s lifestyle with regard to diet and activity and
provide written and oral instructions regarding changes needed while
on warfarin
D. The most common reasons for failure to reach therapeutic levels or
loss of therapeutic control are poor dietary choices and lack of
knowledge about foods high in vitamin K
E. Review the patient’s medications, including any herbal or OTC
medicines, and teach about drug interactions and taking any
medications not approved by the provider
F. Teach the patie nt about signs and symptoms of bleeding and
precautions to take with ADLs while on warfarin (e.g., using soft
toothbrushes and electric razors)
G. If anticoagulation is needed quickly, start with enoxaparin 1
mg/kg/day for the first 5 to 7 days and start warfarin on day 3 while
still on enoxaparin
1. Check INR 3 days after starting warfarin and if near the therapeutic
level, stop enoxaparin and continue warfarin
2. Recheck INR 3 days later
H. The warfarin dose should be taken at the same time each evening and
INR should be drawn in the morning. This allows sufficient time for
the INR results to be obtained and for the patient to be notified of any
changes before taking the evening dose.
I. Baseline laboratory tests
1. CBC
2. INR
3. Chemistry panel to include liver tests and albumin level (warfarin
binds to albumin and if serum albumin is low, a lower dose will be
needed)
VIII. Dosing regimen for special groups; may need to lower the dose at the onset of therapy

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 A. Elderly
B. Malnourished or debilitated
C. Hepatic and renal insufficiency
D. Elevated bleeding risks
E. Concomitant use of p450 inhibitor medications
IX. Reasons for INR fluctuations

A. Has the patient changed the diet or lost/gained weight?

B. Any new or discontinued medications, either Rx or OTC
C. Always confirm the current dose by asking the patient to bring in
current medications in pill bottles and check whether the pills have
changed in shape, color, or size; this can affect the pharmacokinetics of
warfarin and increase or decrease INR, especially if the patient has
stabilized
D. Any recent illness, either short term (e.g., flu) or new long term (e.g.,
cancer)
E. Frequent dosing changes for slightly out-of-range results (it is better to
continue the dose and recheck INR in 5 to 7 days; INR may have
normalized in that amount of time)
F. When a dose has been changed, allow about 2 weeks to reach the
therapeutic range again (unless concerned about INR increasing, then
recheck sooner)
G. When a new medication has been added (or antibiotics started),
recheck INR 3 days after initiation of the new medication and then
about 7 days later to see what effect it will have on warfarin
X. Warfarin reversal guidelines for the management of elevated INR levels (Table 9-3)

A. Typically INR range is 2 to 3; the absolute risk of bleeding remains

fairly low with an INR of <4 but increases with an INR of >4
B. If INR is <9 without a significant bleeding risk, INR can usually be
managed by holding doses until INR normalizes and then restarting
with a decreased dose
C. When using vitamin K (also see Table 9-3)
1. The first dose of vitamin K can be expected to lower INR within 8 to 24

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 hours; a second dose may be required at that time to continue lowering
INR until the therapeutic range is reached
2. If using high doses of vitamin K (e.g., >5 mg) to correct coagulation,
beware that this can lead to warfarin resistance for >1 week and will
increase the risk for thromboembolism. Consider using heparin or
enoxaparin to maintain anticoagulation for 5 to 7 days.
XI. Duration of anticoagulant therapy

A. Low-risk TIA or minor stroke with CHA2DS2-VASC score <1 (see Table
8-9): no therapy related to bleeding risk but may benefit from short-
term antiplatelet therapy
1. ASA 81 to 325 mg + clopidogrel 75 mg qd for 3 weeks then
2. Stop clopidogrel and continue ASA indefinitely (unless
contraindicated)
B. Other chronic cardiovascular diseases based on CHA2DS2VASc score
>1 (CVA with bleeding and AF): suggest ASA + clopidogrel or
clopidogrel alone or daily warfarin with an INR range of 2 to 3
C. DVT/PE
1. First episode with no risk factors: 3 to 6 months if distal DVT; consider
chronic therapy if proximal DVT (causes increased risk of recurrent
DVT)
2. First episode without a cause (idiopathic): 6 to 12 months and consider
daily ASA 81 to 325 mg therapy if no risk factors
3. Recurrent DVT: chronic therapy with warfarin or antiplatelet therapy
4. Hypercoagulable state/malignancy or >2 clots: consider at least 12
months or chronic therapy
5. Status post arthroscopy (hip/knee): start therapy about 24 hours after
surgery and continue for 4 to 6 weeks
6. Valvular disease: chronic therapy
7. Valvular replacement
a) bioprosthetic: 3 to 12 months, followed by ASA therapy indefinitely
b) mechanical: chronic therapy
XII. Preprocedural discontinuation of anticoagulants/antiplatelets (these guidelines are based on

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general recommendations; each institution may have different rules)

A. Hip/Knee replacement: stop warfarin 5 to 7 days before surgery;

usually restarted within 24 hours postop
B. Minor dental procedures: may continue warfarin and ASA; if needed,
can stop 3 days prior and restart 24 hours after the procedure if there is
no significant risk of thrombosis
C. Cataract surgery: no need to stop therapy
D. Elective surgery, if there is a high risk of a cardiac event: stop ASA
and other anticoagulants/antiplatelets about 7 to 10 days before
surgery and restart 24 hours postop when hemostasis is adequate
E. Colonoscopy: stop all anticoagulants/antiplatelets 3 days before the
procedure
XIII. Other anticoagulants not related to warfarin can be used for chronic therapy and postop
procedures that do not require such close monitoring (Table 9-4)
XIV. Contraindications to anticoagulant/antiplatelet medications

A. Pregnancy
B. Active bleeding or within 2 weeks of a major bleeding event
C. Significant hypotension
D. Bleeding that involved the brain, eye, or abdominal cavity
E. History of heparin-induced thrombocytopenia (HIT)
F. End-stage renal disease or creatinine clearance of <30 ml/min
XV. Complications of anticoagulant/antiplatelet medications

A. Bleeding: there are no reversal agents for antiplatelet medications

except for warfarin
B. Heparin-induced thrombocytopenia (HIT)
C. Warfarin-induced skin necrosis
Table 9-2
Titrating Warfarin*

Days to
INR Dose Change
Next INR
1.0- ↑ the dose by 20% 3-5 days
1.1
1.2- Continue the same dose 5-7 days

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 1.5
1.5- ↑ the dose by 10%-15% 5-7 days
1.9
2.0- Continue the same dose 5-7 days
2.5
2.6- Continue the same dose 3-5 days
3.0
3.0- Hold the dose for 1-2 days 2-3 days
5.0
>5 Hold 1-2 doses and consider vitamin K if bleeding risk is elevated (see 1-2 days
Ambulatory Warfarin, VI in this chapter)
*Start
with 5 mg and recheck in 3 days, then follow the table.
Rule of thumb for dose adjustments with an INR of 1.5 to 3.0: if you want to change INR by 0.5 to 1 unit, increase or decrease the
weekly dose by a daily dose. Example: if a patient has been taking 5 mg warfarin daily for at least 2 weeks and INR is still <1.5, add 5
mg to the weekly dose (5 mg M-F and then add 0.5 mg on Sat and Sun); this should increase or decrease INR to between 2 and 3.
Rule of thumb for dosing changes for any INR needing adjustment: calculate the weekly dose and then change by 5% to 20%.
Example: if TWD is 35 mg (based on 7 days), a 10% decrease would be 31.5 mg for the week and the daily dose would change to 4.5
mg; a 10% increase would give 38.5 mg and the daily dose would be 5.5 mg. Recheck INR in about 3 to 5 days after making a change.
You can also round up or down depending on the stability of INR.

Table 9-3
Reversal Guidelines for Elevated INR Levels

INR Action
3-5 with no Hold 1 dose and decrease TWD by 5%; recheck INR in 3 days
bleeding risk
5-9 with no Hold 1-2 doses; recheck INR in 24 h and when INR normalizes, decrease TWD
bleeding risk by 10%
5-9 with Hold 1-2 doses, give vitamin K 1.25-5 mg orally and recheck INR in 24 h; repeat
bleeding risk* vitamin K if INR not normalized; ↓ the TWD dose by 10%-15%.
5-9 with need Send to ED; if available, give vitamin K 5-10 mg
to rapidly
reverse effects
>9 with no Hold warfarin, give vitamin K 5-10 mg orally; recheck INR in 24 h and repeat
bleeding risk dose of vitamin K if needed; when INR normalizes, restart warfarin at
10%-15% less TWD; recheck INR q24h until normalized
>9 with Send to ED
bleeding risk
or bleeding
present
*
The risk factors for bleeding include the following: history of GI bleeding, uncontrolled HTN, unstable cerebrovascular disease, ischemic
CVA, HF, renal insufficiency, age >75 years, recent surgery, dehydration, platelet disorders, and excessive alcohol use. The most
common sites for bleeding are the GI tract, GU tract, and soft tissues.

Table 9-4
Indications for Ambulatory Anticoagulation/Antiplatelet Drugs (Excluding Warfarin)

Drug Dose Indication

Apixaban (Eliquis) (anticoagulant) 5 mg bid DVT/PE treatment and stroke prophylaxis
Oral administration 2.5 mg Prophylaxis s/p hip replacement for 32-38
2.5-5 mg days
Prophylaxis s/p knee replacement for 10-14

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 days
Nonvalvular AF, start at a lower dose

Dabigatran (Pradaxa) (anticoagulant) 150 mg bid Nonvalvular AF

Oral administration CVA
Prophylaxis s/p hip replacement for 28-35
days
Prophylaxis s/p knee replacement for 10 days

Rivaroxaban (Xarelto) (anticoagulant) 10 mg Prophylaxis s/p hip replacement for 35 days

Oral administration 20 mg Prophylaxis s/p knee replacement for 12 days
DVT/CVA, initial and recurrent
Nonvalvular AF

Clopidogrel (Plavix) (antiplatelet) 75 mg daily ACS or recent MI

Oral administration CVA
PAD

Prasugrel (Effient) (antiplatelet) 10 mg qd based on cardiac Unstable angina

event
Oral administration Non–ST-elevation MI
STEMI undergoing PCI

Ticagrelor (Brilinta) (antiplatelet) 90 mg bid* Unstable angina

Oral administration ACS
Non–ST-elevation MI
STEMI

Fondaparinux (Arixtra) (anticoagulant) 2.5 mg Prophylaxis s/p hip replacement for 5-9 days
SQ administration 2.5 mg Prophylaxis s/p knee replacement for 5-9 days
Short term use; overlap with warfarin 5-10 mg (based on weight) DVT/PE treatment
therapy

Enoxaparin (Lovenox) (anticoagulant) 1 mg/kg q12h DVT treatment and prophylaxis

SQ administration STEMI
Short term use; overlap with warfarin Unstable angina
therapy

Heparin (anticoagulant) 5000 units Thromboembolism prophylaxis

SQ or IV administration 18 mg/kg/h Thromboembolism treatment
Short term use; overlap with warfarin
therapy

*Must limit ASA to <100 mg/day.

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Chronic wound management
Chronic wound care

I. Chronic wounds occur because of tissue damage from pressure on the skin over bony surfaces
or decreased blood supply

A. Occur commonly in bedridden, malnourished, and elderly people and

those with peripheral vascular disease
B. The weight of the pressure is not as important as the length of time the
pressure is present over a compromised area
II. Remodeling and scar formation occur over 3 weeks to 2 years; the strength of the scar is only
about 80% of the original skin strength
III. Diagnostic studies to consider before treatment

A. CBC, chemistry profile with albumin and protein ratios

B. A1c, coagulation studies, and wound cultures
C. ABI to determine arterial circulation (see Calculation of ABI in this
chapter)
D. X-ray of the area involved; CT or MRI may be indicated to determine
the underlying etiology and any bone involvement
E. Ultrasound of suspect arterial system to identify aneurysm or DVT
F. Bone scan to identify osteomyelitis
IV. Documentation of wound description

A. Size and depth, any undermining present

B. Appearance of the wound surface (wound edges, color) and wound
bed
C. Amount of exudate, color, and odor
D. Tissues surrounding the wound bed

Differentiation of wounds

I. Venous ulcers: caused by venous insufficiency and varicose veins

A. Description
1. Wounds are usually found over bony prominences (e.g., medial

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 malleolus); the edges are pink with granulation and the base is moist
with moderate-to-heavy exudate. The surrounding skin is often
reddish-brown (i.e., brawny) brawny in color.
2. Feet are warm with normal pulses and sensation
B. Treatment
1. Keep the wound bed moist and change dressings appropriately for the
amount of exudate; protect the surrounding tissue from maceration
2. Debride any necrotic tissue by surgical, autolytic, or enzymatic
methods; short term use of wet to dry dressings may be effective
3. Monitor for infection and treat aggressively if identified; the signs of
infection may differ with chronic wounds
a) the wound may increase in size and be malodorous and/or have
friable granulation tissue
b) delayed wound healing and tunneling
c) may see signs of sepsis (especially in elderly people) with fever, chills,
tachycardia, and leukocytosis
4. Elevation of the extremity
5. Compression stocking therapy (see Compression Stocking Therapy in
this chapter)
6. Drug therapy
a) initially begin broad-spectrum antibiotics, followed by a specific
antimicrobial depending on the culture and sensitivity
b) consider topical antimicrobials, which fall into two categories
(1) antiseptics have a broad antimicrobial spectrum but may be harmful
to the tissue; commonly used antiseptics are hydrogen peroxide,
chlorhexidine, betadine, and silver-releasing agents
(2) topical antibiotics usually have more specific cellular targets and a
narrower spectrum of activity; may induce contact dermatitis; are
more likely to induce bacterial resistance; most commonly used are
bacitracin, neomycin, mupirocin, retapamulin, gentamicin, and fusidic
acid
7. Assess tetanus prophylaxis because wounds are an entry portal for

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 Clostridium tetani
C. Refer for surgical grafting for wound closure or to a wound care clinic
II. Pressure ulcers

A. Description
1. Occur with prolonged pressure over areas of higher impact and over
bony prominences; can occur as a result of the shearing effect (sliding
up or down in bed and turning)
2. Wounds may begin very subtly as reddened areas that progress to
avascular white areas and then to skin degradation and ulcer
formation (see Wound Staging and Description in this chapter)
B. Treatment
1. Treat according to the stage (see Wound Staging and Treatment in this
chapter)
2. Remove the cause of pressure, which may resolve any tissue damage;
use pillows, supportive limb devices, and off-loading pressure
mattresses/beds
3. Keep the head of the bed at the lowest effective level to prevent
shearing from movement while in bed
4. Frequent turning schedules; usually q2h with documented rotation
charts
5. Manage bowel and bladder incontinence to prevent further skin
breakdown and infection
6. Improve the nutritional status and supplement with vitamin C, zinc,
and multivitamins
C. Refer to a wound care specialist or a surgeon if wounds become
resistant to treatment
III. Arterial insufficiency ulcers

A. Description: these ulcers are usually chronic

1. Usually caused by ischemia in the extremity because of poor
circulation, poor control of DM or injury to already compromised skin
from surgery or past wounds
a) skin reddens with dangling and turns pale white with elevation

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 (differentiates this from venous wounds)
b) wounds are usually found at the ends of extremities (toes, heels,
between toes, lateral malleolus, and phalangeal heads)
c) ulcers appear deep with even edges and a dry, grayish base with
nonerythematous borders; there is no granulation tissue and the skin
around the ulcer is shiny and thin
2. Additional signs and symptoms
a) history of claudication symptoms
b) rest pain is usually present
c) acute pain that is worse at night and described as sharp or burning; the
extremity is usually cold
d) atrophy of the skin, with hair loss over the affected extremity
e) decreased or absent pulses with paresthesia
B. Treatment
1. Meticulous wound and foot care
2. Whirlpool treatments to improve circulation and maintain cleanliness
3. Short-course systemic antibiotics (routine antibiotic use is discouraged)
4. Dressing should maintain a moist wound bed and be changed q1-2d
C. Refer to a wound care specialist or a vascular surgeon if no
improvement is seen in 2 to 4 weeks

Wound staging and treatment

I. Stage 0 (red stage)

A. Clean, healthy granulation tissue; initial layers of tissue begin as pink,

then proceed to beefy red
B. Treatment is to maintain pressure-alleviating environment
II. Stage 1 (early localized erythema)

A. Nonblanching erythema of intact skin; this is the heralding lesion of

skin ulceration
B. Aggressive therapy with hydrocolloid (Duoderm) q2-3d for 14 days
and remove all pressure to the area and decrease edema

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III. Stage 2 (red-to-yellow ulcer)

A. Partial-thickness skin loss involving the epidermis, dermis, or both;

superficial ulcer that presents clinically as an abrasion, blister, shallow
crater, or crack
B. Treatment involves cleansing with saline, then applying hydrocolloid
(Duoderm) q2-3d for 45 days (often performed by wound care
specialist). Alleviate all pressure to the area and decrease edema. Use
pressure-relieving mattresses/beds.
IV. Stage 3 (yellow ulcer)

A. Full-thickness skin loss involving damage to or necrosis of the

subcutaneous tissue that may extend down to but not through the
underlying fascia
1. The ulcer at presentation is a deep crater with or without undermining
of the adjacent tissue; distinct ulcer margin
2. The exudate can be whitish yellow, greenish yellow, or beige
3. Sloughing tissue is present, indicating the presence of microorganisms
and need for cleaning
B. Treatment is debridement, irrigation with saline and hydrocolloid
(Duoderm) q2-3d for 90 days, and monitoring for infection (often
performed by wound care specialist). Start nutritional support with
increased vitamin C, zinc, and multivitamins.
V. Stage 4 (black ulcer)

A. Eschar or necrotic tissue present over the wound with full-thickness

skin loss, extensive destruction, tissue necrosis, and/or damage to
muscle, bone, or supporting structures
1. This should be removed as soon as possible because it is an excellent
medium for bacterial growth and decreases the wound-healing process
(the exception is heel eschar, see Practice Pearls for Wound Care)
2. Undermining (tunneling) and sinus tracts are usually involved later in
the wound process
B. Treatment includes superficial debridement, irrigation with pressure,
and topical dressing depending on the amount of exudate or amount
of eschar (often performed by wound care specialist)

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 P r a c t i c e Pe a r l s f o r W o u n d C a r e

• When describing wounds, document the size (in cm or mm), location of the primary wound,
any undermining or tunneling, color of the wound and the skin around the wound, and any
odor.
• Treat the underlying disease(s) aggressively and improve the nutritional status with
increased vitamin C, prenatal vitamins, zinc, and vitamin E.
• Adequate O2 level is needed for tissue healing.
• Protect the lower extremities by using sheepskin wraps with Velcro to surround the leg from
the knee to the ankle; these wraps are warm and nonconstricting.
• If the extremity shows evidence of edema, use diuretic therapy and limb elevation. Edema
will impede healing if not resolved.
• Compression stockings on the lower extremity are beneficial if they can be applied without
skin injury.

• Application of Ace-wraps can be used if the staff member or family

member is skilled in application.
• Monitor skin integrity with every application.
• Rule out DVT in case of a single edematous extremity.
• Protein-rich fluid retains a “pit” when depressed 1 mm, suggesting cardiac disease (HF);
protein-poor fluid with “quick spring back” when depressed is suggestive of hepatic or
renal disease or malnutrition.
• Wound infections may be colonized by opportunistic bacteria.
• Superficial wound infection is characterized by foul-smelling exudate, poor tissue
appearance, increased exudate, increased pain, crepitus, necrosis, and lymphadenopathy;
systemic infection is characterized by fever, chills, leukocytosis, and increased sed rate.
• Dry heel eschar without evidence of infection (e.g., edema, redness, or exudative discharge)
should be left alone and monitored q1wk.

• Paint heels with betadine 1 to 2 times a day.

• Use protective wraps to minimize any type of pressure while the
patient is in/out of bed.
• Use air pressure or pressure release beds with cutout heel protectors
while in bed.
• Remove any foreign objects from the wound.
• Irrigate wounds with normal saline only; if the surface is exudative, irrigate under pressure
using a 20-ml syringe with an 18-g needle and amount of force needed to loosen debris.
• After debridement or irrigation, provide a moist wound bed with saline gel dressing
(Normlgel, Intralite gel) or hydrocolloid agent (Duoderm).

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• Wet-to-dry dressings enhance autolytic debridement.
• Whirlpool treatment should be used for large surface wounds with exudate.
• Avoid hydrogen peroxide, betadine, acetic acid, and Dakin’s solution for long periods of
time because of tissue toxicity, although betadine may be used to loosen and separate eschar
and maintain sterility of the wound and surrounding area.
• Refer to a wound care specialist for wounds that are enlarging, tunneling, have foul odor,
and are not responding.

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Anemia
I. Anemia is a sign of a disease (not a diagnosis) that causes a decrease in RBC, Hgb, or Hct,
making it more difficult for the remaining cells to carry O2 to body tissues
II. Definition: anemia is generally defined as follows:

A. Infants and children: Hgb <11 g/dl

B. Women: Hgb <12 g/dl
C. Men: Hgb <13 g/dl
III. Causes

A. Loss of circulating RBCs and inability of the body to rebuild the RBC
volume in a timely manner
1. Caused by emergent blood loss through GI tract, surgery, or injury
2. Slower continuous losses are from menstrual bleeding, GI polyps, or
small ulcers
B. Overdestruction of RBCs
1. Hemolytic anemia from inherited disorders such as sickle cell disease
or thalassemia
2. Acquired hemolytic anemia caused by autoimmune diseases, malaria,
or hemolytic uremic syndrome
C. Inadequate production of RBC
1. Lack of or malabsorption of certain nutrients needed to produce
healthy RBCs (i.e., iron, folate, or B12)
2. Bone marrow disorder resulting in lack of cell production
3. Inadequate production due to decreased use of iron and/or shortened
lifespan of RBCs is usually secondary to malignancy or chronic illness
IV. Interpreting the CBC to determine the probable cause of anemia

A. Step 1: start with the RBC count; if this is low, the number of
circulating RBCs is deficient
B. Step 2: Hgb and Hct
1. Hgb is the protein component of RBC that carries O2, and Hct is the
percentage of RBCs in the blood volume

314
2. If these are low, there will be a deficiency in the O2-carrying capacity of
the cell, which is exacerbated by RBC deficiency
C. Step 3: Mean corpuscular volume (MCV) measures the average size of
RBCs. This is the most useful value to help classify the type of anemia.
1. MCV >100 fl (macrocytic) indicates increase in RBC size, which may be
related to
a) abnormal RBC maturation (myelodysplastic syndrome, leukemia)
b) abnormal metabolism of RBC precursors (folate or B12 deficiency;
MCV usually >105 fl)
c) alcohol abuse, liver disease, and hypothyroidism
d) MCV between 100 and 105 fl: consider alcohol-related cause
2. MCV <77 fl (microcytic) indicates decreased cell size which may be
related to
a) blood loss (either rapid or slow); there is an inability to produce the
required amounts of blood cells
b) iron deficiency anemia, thalassemia, low serum ferritin, and chronic
disease
3. MCV 80 to 100 fl (normocytic) is considered normal and can be seen in
anemia of chronic disease, renal disease, acute blood loss, aplastic
anemia, and hemolytic (autoimmune) anemias
D. Step 4: The ability of the bone marrow to increase the production of
reticulocytes (immature RBCs) in response to anemia is called
reticulocyte production index (RPI). This calculation is based on the
number of days needed to release reticulocytes from the bone marrow
into circulation.
1. Normal RPI is 2 to 3
2. Elevated RPI (>3) indicates active bone marrow response to
compensate for blood loss, hemolysis, or bone marrow response to
therapy
3. Low RPI (<2) indicates decreased production and could be related to
aplastic or megaloblastic anemia; is seen in bone marrow failure, iron
deficiency, vitamin B12 deficiency, lead poisoning, or anemia of
inflammation

315
 4. The following formula is used to calculate the reticulocyte production
index (RPI) on the basis of lab retic value, patient Hct ÷ 45 (normal
Hct), and maturation correction for retic production in days Retic
count % × (Pt Hct/45) × maturation correction = RPI

HCT Maturation correction in days

45 1 day
35 1.5 days
25 2 days
15 2.5 days

E. Step 5: Red cell distribution width (RDW) measures variations in red

cell width
1. Elevated RDW is indicative of nutritional deficiency (e.g., iron, folate,
vitamin B12)
2. Can help further delineate between megaloblastic anemia and other
causes
3. Compared with MCV, it can help to narrow the diagnosis for the cause
of anemia
a) normal RDW with
(1) low MCV: anemia of chronic disease or α-or β-thalassemia
(2) normal MCV: acute blood loss, anemia of chronic disease, or renal
disease
(3) elevated MCV: aplastic anemia or chronic liver disease,
chemotherapy, alcohol, or viral infections
b) elevated RDW with
(1) low MCV: iron deficiency, sickle cell, or β-thalassemia
(2) normal MCV: early Fe, folate, or B12 deficiency; sickle cell disease;
chronic liver disease; myelodysplastic syndrome
(3) high MCV: folate or vitamin B12 deficiency, immune hemolytic
anemia, chronic liver disease, myelodysplastic syndrome, and thyroid
disease
F. Step 6: Tests to help further determine the cause of anemia
1. Iron (Fe) level is the amount of iron bound to transferrin and able to
bind to Hgb and carry O2

316
a) elevated Fe: consider pernicious anemia, thalassemia, lead poisoning,
estrogens, or excessive iron intake (e.g., multiple transfusions or excess
iron replacement)
b) decreased Fe: consider Fe-deficiency anemia, hypothyroidism,
malignancy, chronic renal failure
2. TIBC: cells that carry iron
a) increased TIBC: consider Fe deficiency, liver damage, blood loss,
progesterone birth control pills
b) decreased TIBC: consider hemochromatosis, hemosiderosis,
thalassemia, hyperthyroidism, anemia of chronic disease
3. Ferritin: the storage protein for iron; correlates with the total body
stores of iron
a) increased ferritin level: consider liver disease, infection, alcoholism,
hyperthyroidism, iron overload, ESRD
b) decreased ferritin level: consider Fe deficiency and hemodialysis
4. B12 levels
a) deficiency caused by significant loss of the stomach mucosa (e.g.,
secondary to gastric bypass) that prevents absorption of B12,
decreased production of intrinsic factor (commonly seen in elderly
people), or lack of B12 intake (vegan diets, alcoholism, and long-term
use of acid-reducing drugs)
b) long-term deficiency results in dementia, peripheral neuropathy,
megaloblastic anemia
5. Folate levels: causes of deficiency include alcohol abuse; elderly; poor
dietary intake of animal proteins, vegetables, and fruits; vegetarian or
fad dieters and people with pernicious anemia may have elevated
levels
6. Methylmalonic acid (MMA) is elevated in vitamin B12 deficiency and
is more sensitive than testing vitamin B12 serum levels (especially in
elderly people)
7. Lactate dehydrogenase (LDH) can be used to help identify RBC
breakage due to fragility or destruction (e.g., artificial heart valves);
can be seen with hemolytic anemia

317
 G. Step 7: Urinalysis for hematuria and stool for occult blood
H. Step 8: By this time, you should have a good idea of the cause of
anemia and what referral is needed

P r a c t i c e Pe a r l s f o r A n e m i a

• With anemia of blood loss in women aged ≥50 years or postmenopausal, it is a good idea to
perform pelvic U/S, especially if this is a new anemia; if the findings are normal, consider
EGD/colonoscopy.
• With anemia of blood loss in men, obtain EGD and/or colonoscopy and PSA.
• Symptoms can be sudden or slow to manifest and often become noticeable only when there
is an increased demand for O2 with activity.

• Patients with mild anemia are often asymptomatic and may only
complain of fatigue, DOE, or palpitations after exercise or exertion; as
anemia progresses, the symptoms will worsen.
• In less severe anemia or chronic long-term anemia (Hgb <10 g/dl),
symptoms will be compensated and pallor may be the presenting
symptom with c/o fatigue.
• In severe anemia (Hgb <7 g/dl), the resting cardiac output rises with an
increase in both the heart rate and stroke volume, resulting in
tachycardia and widened pulse pressure. These signs may be present
at rest as anemia progresses.

Anemia secondary to blood loss

I. Acute blood loss: usually caused by a significant loss of the blood volume either internally (GI
bleed) or externally (trauma), which leads to hypoperfusion of organs

A. Signs and symptoms

1. Fatigue, feeling of “doom,” and dizziness, especially with position
changes
2. Rapid-onset tachycardia, tachypnea, diaphoresis, pallor, cyanosis,
hypotension, and evidence of bleeding
3. May not see changes in Hgb/Hct for 24 to 48 hours with acute blood
loss, but after that, will see decreased Hgb/Hct, MCV, and iron levels

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 B. Treatment involves stabilization and transport to nearest ED
1. After stabilization and release from hospital, monitor CBC, ferritin, and
iron monthly until stable
a) start iron supplementation with OTC iron supplements (see Fe-
deficiency anemia)
b) iron-rich foods (see Appendix A)
c) start extra vitamin C, especially with OTC iron supplements (this
improves absorption of iron)
2. Monitor activity levels because there should be an improvement in
stamina
II. Iron deficiency anemia: a microcytic anemia caused by slow blood loss, inability to absorb iron,
or dietary deficiency

A. People at risk
1. Infants and children with whole milk diets and deficiencies in iron-
fortified formulas or foods
2. Adolescents on “fad” diets because they may exclude iron-rich foods
3. Pregnant or menstruating women, impoverished or elderly people
4. Chronic ASA/NSAID users
5. With cancer or at risk for lead poisoning
6. After weight loss/gastric bypass surgeries
B. Signs and symptoms
1. May have no signs or symptoms until Hgb <10 g/dl if blood loss is
slow
2. Pallor in hand creases and circumoral pallor are usually noticeable
when Hgb is <7.5 g/dl
3. Conjunctival pallor and cyanosis (more noticeable in African-
American patients)
4. Systolic murmur and new-onset venous hum
5. Easily fatigued and unable to perform ADLs or work
6. Dizziness with position changes, DOE, leg cramps with exertion
7. Initially mild-to-moderate tachycardia, tachypnea, and palpitations

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 with ADLs; worsens as anemia progresses and will occur at rest
8. Brittle hair and spoon-shaped nails (koilonychia); angular stomatitis
and glossy tongue
9. Pica, especially of ice, is often noted, but the ingested substance can
depend on the population
C. Pertinent laboratory findings: best tests for iron-deficiency anemia are
MCV and ferritin

Test Finding
RBC Decreased
Hgb/Hct Decreased
MCV Decreased
RPI Normal to decreased
RDW Increased
Iron Decreased
TIBC Increased
Ferritin Decreased

D. Treatment is aimed at finding the cause and correcting the problem

1. Begin OTC oral iron replacement, with goal of 60-100 mg of elemental
iron qd
a) ferrous sulfate extended release 325mg bid
b) ferrous gluconate 325 mg 2 tabs bid
c) ferrous fumarate 325 mg 1 tab qd
2. Give with vitamin C to enhance the absorption of the iron product
3. Therapy is continued for 2 to 3 months after Hgb and ferritin levels are
normal
4. Recheck Hgb/Hct, ferritin, and RPI in 1 month and then q6mo for 1
year
5. Diet should be enriched in high-iron foods (see Appendix A): one
serving with each meal
6. Use a stool softener (Colace) 1 to 2 cap qd-bid while taking iron
replacement
E. Refer to a hematologist or gastroenterologist if the patient is
unresponsive to treatment

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Anemia due to inadequate production
I. Anemia of chronic disease (ACD): chronic normocytic anemia seen with inflammatory, infectious,
or neoplastic disorders

A. It is associated with decreased availability of iron to the cells in the

presence of adequate TIBC and ferritin
B. Chronic inflammation causes iron retention by the endothelial system,
which limits the availability for erythropoiesis
C. Signs and symptoms: similar to Fe deficiency but associated with a
chronic disease process
D. Pertinent lab findings: best tests for ACD are iron and TIBC

Test Finding
RBC Decreased
Hgb/Hct Mildly decreased at 10/24
MCV Normal to decreased
RPI Normal to decreased
RDW Normal
Iron Low
TIBC Normal to decreased
Ferritin Normal to increased

E. Treatment: aimed at identifying and controlling the underlying

disease process
1. Transfusions may raise Hgb temporarily and improve the patient’s
quality of life
2. Treatment with iron replacement therapy and erythropoietin therapy
will improve anemia symptoms
3. Recheck CBC and Fe monthly until normalized, then q3-6mo until
stabilized, and then yearly
F. Refer to a hematologist if unresponsive to therapy
II. Pernicious anemia is due to a loss of intrinsic factor (IF) in the stomach mucosa needed to
absorb B12

A. Causes
1. Total or partial gastrectomy, bariatric surgery
2. Gastric cancer
3. Autoimmune diseases with antibodies against parietal cells and

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 intrinsic factor
4. Chronic hemolytic anemia
5. Can have concomitant folate deficiency secondary to decreased
intestinal folate absorption; seen predominantly in elderly people,
alcoholics, and pregnant women
6. Women aged >60 years and vegans who do not take B12 or folate
supplements
7. Renal or liver cancer; hypothyroidism/thyroiditis
8. Medications affecting B12 absorption and/or production
a) chronic PPI use
b) TMP/SMX and sulfa-type medications
c) dilantin
d) barbiturates
e) triamterene
B. Signs and symptoms
1. Classic triad: weakness, paresthesia, and beefy, red painful tongue
2. Gait problems related to advanced disease and loss of joint position
sense
3. Absent or decreased reflexes
4. Confusion and memory loss; depression and dementia
5. Weight loss and anorexia
6. Hepatosplenomegaly
C. Pertinent lab values

Test Finding
RBC Normal
Hgb/Hct Normal to slightly decreased
MCV Increased at 115
(105-109 usually indicative of alcoholism)
RPI Decreased
LDH Increased
B12 level Decreased
MMA Increased with B12 deficiency
Normal with folate deficiency

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 Folate Normal or decreased
Homocysteine Increased with both folate and B12 deficiency

D. Treatment
1. Lifetime supplementation with deficient vitamin
a) B12 replacement
(1) cyanocobalamin 1000 mcg/day IM for 5 days, then 1000 mcg/wk for 4
weeks, then q1mo
(2) cyanocobalamin nasal (Nascobal) 500 mcg/spray in one nostril every
week
(3) cyanocobalamin orally 1000 µg daily (requires IF for absorption)
b) recheck vitamin levels in 4 weeks and again in 8 weeks
(1) increase dietary sources of vitamin B12
(2) symptoms will resolve quickly if deficiency is of a short duration
(3) advise the patient of an increased risk of esophageal, pancreatic, and
rectal cancer associated with B12 deficiency
III. Folate deficiency is a lack of folic acid, a water-soluble B vitamin required for normal RBC,
protein, and DNA production

A. Causes
1. Poor dietary intake of foods containing folic acid (see Appendix A);
commonly seen in the elderly, poor, and people who do not eat
vegetables or fruits
2. Celiac disease (poor absorption)
3. Increased alcohol intake
4. Hemolytic anemia
5. Medications: dilantin, sulfasalazine, TMP/SMX
B. Signs and symptoms
1. Fatigue
2. Mouth ulcers and swollen tongue
3. Graying hair
4. Poor growth

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 C. Treatment is for lifetime
1. Increase in the dietary intake of appropriate foods (see Appendix A)
2. Folic acid 1 mg/day po
IV. Myelodysplastic syndrome: caused by bone marrow dysfunction affecting the production of one
or more cell lines; more common in elderly people and can be a precursor to leukemia

A. Signs and symptoms: may be proceeded by “years” of unexplained

mild decrease in platelets and neutropenia with anemia
1. Fatigue and malaise
2. Petechiae, ecchymosis, bleeding from the gums and nose
3. Fever, cough, dysuria, and UTIs
B. Pertinent lab values

Test Finding
RBC Decreased
Hgb/Hct Decreased
MCV Increased >100 fl
RPI Decreased
RDW Normal to increased
Platelets Decreased
WBC Decreased
LDH Increased

C. Treatment
1. Refer to a hematologist for chronic care
2. Transfusions (PRBC) may be required periodically

Anemia secondary to overdestruction

I. Thalassemia (minor and major) is a genetic RBC synthesis abnormality; the person usually has a
family history of mild, unexplained anemia

A. Signs and symptoms

1. Thalassemia major (i.e., β-thalassemia) is usually identified in early
childhood with severe symptoms of anemia; β-thalassemia minor
(trait) is less severe with microcytic anemia
2. Symptoms similar to iron deficiency with mild pallor but unresponsive
to iron replacement
3. Breathlessness and poor exercise tolerance

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 4. Splenomegaly (usually requires splenectomy)
5. Cholelithiasis is common (usually requires removal of gallbladder
secondary to stones)
6. Growth retardation, failure to thrive, and jaundice in severe β-
thalassemia major
B. Pertinent lab values (reflective of thalassemia minor)

Test Finding
RBC Normal to slightly increased with unusual red cell morphology (more unusual in
thalassemia major)
Hgb/Hct Mildly decreased (≤10 g/dl)
MCV Decreased
RPI Decreased
RDW Normal to elevated
Iron Increased
WBC May be highly elevated in β-thalassemia

C. Treatment
1. Referral to a hematologist for monitoring
2. Monitor iron levels and do not give supplements with iron; restrict
iron-rich foods
II. Sickle cell anemia (SCA)

A. An autosomal recessive inherited disease caused by abnormally

shaped RBCs causing an inability to carry O2; this can manifest as
sickle cell disease or sickle cell trait
1. Because of the odd shape and fragility of the RBC, it is destroyed early
and the bone marrow cannot keep up with the demand found in sickle
cell disease
2. Sickle cell trait is a carrier state; the person usually does not have
symptoms of SCA but predisposes his or her children to SCD
3. Predominantly found in populations of Afro-American,
Mediterranean, and Central African descent
4. Usually found at birth with screening tests; severity varies
B. Signs and symptoms
1. Vaso-occlusive illness with symptoms related to the inability of RBCs
to pass through small capillaries, causing severe joint pain, swelling,

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 chest pain, and splenic sequestration (which could lead to rupture)
2. Hand and foot edema; bone pain
3. Signs of IDA (see iron-deficiency anemia)
4. Pulmonary HTN
5. Growth retardation
6. CVA and intracranial bleeding
C. Pertinent lab values

Test Finding
RBC Decreased
Hgb/Hct Mildly to moderately decreased
MCV Mildly to moderately decreased
RPI 3-4 times the upper normal limit
RDW Increased
Platelets Increased
WBC Increased
LDH Increased

D. Treatment
1. Refer for management by a hematologist or specialist in SCA
2. Analgesia (may require daily or intermittent narcotic medications to
control symptoms and maintain quality of life)
3. If in an area that treats a number of SCA patients, refer to local
protocols for management of crisis and general care
4. Monitor immunization updates
III. Autoimmune hemolytic anemia: an acquired anemia that causes the immune system to produce
antibodies against RBCs; there is no known reason for the disease

A. Certain conditions increase the risk

1. SLE
2. Leukemia
3. EBV, CMV
4. Hepatitis, non-Hodgkin’s lymphoma
5. HIV/AIDS
6. Blood transfusions

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 B. Signs and symptoms
1. Fatigue, DOE
2. Pallor
3. Dizziness, palpitations, tachycardia, and tachypnea
4. Chest pain, HF
5. Jaundice, dark urine, sclera icterus
6. Hepatosplenomegaly, gallstones
C. Pertinent lab values

Test Finding
RBC Decreased; morphology positive for spherocytes
Hgb/Hct Decreased
MCV Increased
RPI Increased
RDW Normal to increased
Direct Coombs test Positive
LDH Increased

D. Treatment: refer to a hematologist for further care

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CHAPTER 10

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Abdominal conditions
For details regarding complete history and physical examination, see Chapter 1.

Focused abdominal examination

I. With abdominal complaints, keep the initial focus broad; symptoms inconsequential to the
patient may be important
II. A complaint of abdominal pain requires more focused examination related to the cause of the
pain
III. The source of abdominal pain may be difficult to pinpoint because of the involvement of
various organs

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 Differential Diagnosis of Abdominal Problems Depending on Pain
Location Source: (From Lewis SL, Dirksen SR, Heitkemper MM, Burcher L: Medical-
Surgical Nursing, ed 9, St. Louis, 2014, Elsevier.)

Abdominal pain (table 10-1)

I. Parietal pain

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 A. Causes
1. Pain is well localized and intense, caused by ischemia, inflammation,
or stretching of the parietal peritoneum
2. Can be related to solid organ inflammation/infection; solid organs are
insensitive to pain, but the inflammatory process causes stretching
around the origin of the painful region, which causes pain to be
perceived in the peritoneum
B. Description
1. Pain is steady, constant, and described as “sharp,” “knifelike,” and
“constant”
2. Will have abdominal tenderness, guarding, rebound tenderness, and
rigidity
3. Pain is relieved with legs up in the fetal position
4. Pain is aggravated by cough or movement
C. Examples of this type of pain
1. Abdominal aortic aneurysm (AAA)
2. Appendicitis, cholecystitis, pancreatitis
3. Diverticulitis, perforation of the gut, peritonitis
II. Visceral pain

A. Description: pain is described as dull and poorly localized, cramping,

colicky, or gnawing with burning sensation and is usually felt in the
midline of the abdomen
B. Examples
1. Mesenteric ischemia, splenic rupture
2. Pancreatitis
3. Gastroenteritis
4. Pregnancy, ectopic pregnancy
5. Kidney stones, bladder, UTI
6. Obstruction in the colon, ileus
III. Referred pain

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 A. Caused by both visceral and spinal components because of shared
central pathways from different locations; it is described as both vague
and local pain
B. Examples
1. AAA: pain felt in the back, flank, abdomen, and groin
2. Appendicitis: pain felt in the epigastrium, periumbilical region, and
right lower quadrant
3. Cholecystitis: pain felt in the epigastrium, RUQ, and right scapula
4. Pancreatitis: pain felt in the epigastrium, abdomen, back, and flanks
5. Ectopic pregnancy: generalized pain felt in the abdomen and either
shoulder
6. Splenic rupture: pain felt in the RUQ, abdomen, and left shoulder
IV. Surgical considerations

A. With acute abdominal pain persisting for >6 hours, followed by nausea
and vomiting
B. If nausea and vomiting occur before pain, this is most likely a medical
problem
C. Elderly patients with abdominal pain will possibly require surgery
unless an obvious cause is found (e.g., UTI or constipation)
D. With pediatric patients, the further the pain is from the umbilicus, the
more likely the pain is from acute abdomen; pain at the umbilicus is
often associated with constipation or functional abdominal pain
E. If you think someone is feigning abdominal pain, press into the
abdomen with hands while listening with a stethoscope; if pain is not
present with this maneuver, then the likelihood of a real surgical
problem decreases. Observe for wincing and guarding during
examination.
V. Physical examination techniques related to the cause of pain

A. Observation/inspection
1. If the patient is lying very still (because of pain): consider peritonitis
2. If the patient is writhing about on the bed (in pain): consider intestinal,
colicky pain from a hollow organ such as kidney stone, gallbladder

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 disease, AAA
3. If the abdomen is distended and firm: consider bowel obstruction or
perforation
B. Auscultation
1. If bowel sounds are absent: consider peritonitis
2. If bowel sounds are high pitched or absent: consider bowel obstruction
C. Percussion
1. Resonant, shifting dullness usually indicates ascites
2. If percussion causes pain: consider peritonitis
D. Palpation (examine tender areas last)
1. During palpation, try to visualize which organs are being palpated and
the surrounding organs; this will help you identify what abnormalities
or masses may be present
2. To determine whether a mass involves the abdominal wall or is
intraabdominal, have the patient raise his/her head unsupported
a) a mass in the abdominal wall will become more obvious with tensing
of the abdominal muscles and will be more obvious on inspection
b) an intraabdominal mass will become less obvious because the muscles
will push the mass down below the muscle wall
3. Guarding is voluntary contraction of abdominal muscles and tends to
be generalized
4. Rigidity is involuntary tightening of abdominal muscles and tends to
be localized over the inflamed area (rigidity is a positive sign of
peritoneal inflammation)
5. When examining a child, have the child place his/her hand over yours
and gently push down while you move your hand to palpate for
organs. This allows the child to have some control and reduces fear
and ticklishness in the child.
E. Techniques to identify peritoneal signs indicating “acute abdomen”
that would require further evaluation and possible surgical
intervention
1. Psoas sign: have the patient flex his/her thigh against resistance or

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 with the patient lying on the left side, hyperextend the right thigh
against resistance. If pain is elicited, this would be indicative of
peritoneal irritation.
2. Obturator test: with the patient supine and knee flexed 90° with the
foot on the bed, immobilize the ankle on the bed and internally and
externally rotate the hip. If pain is elicited, this would be suggestive of
pelvic abscess or appendicitis.
3. Markle’s sign (heel jar test): have the patient stand on toes and then
forcefully drop down onto heels or have the patient in a supine position
on the bed while the examiner firmly taps the heel with the ball of the
hand. If pain is elicited, this is suggestive of appendicitis or peritoneal
irritation.
4. Rovsing’s sign: palpation in the LLQ causes pain in the RLQ; this is
suggestive of peritonitis or appendicitis
5. Cullen’s sign: yellow-blue discoloration around the umbilicus
suggestive of acute pancreatitis, ectopic pregnancy, or internal
hemorrhage
6. Grey-Turner’s sign: bruising on the flanks associated with
hemorrhagic pancreatitis, retroperitoneal hemorrhage, or blunt trauma
7. Kehr’s sign: severe left shoulder pain due to blood or pus in the
peritoneal cavity, usually from ruptured spleen
8. Murphy’s sign: firmly place a hand at the costal margin in the RUQ
and ask the patient to breathe deeply. If the gallbladder is inflamed,
this will cause pain and the patient will “catch his/her breath” as the
gallbladder descends under the hand, indicating inflammation.
9. Carnett’s sign: have the patient lie flat with the head lifted up and with
chin close to the chest (or shoulder off the bed); this will tighten the
abdominal muscles. Pain elicited with this test is usually from the
abdominal muscle wall; if pain decreases, this indicates that pain is
from intraabdominal structures.
F. Further examination techniques/tests
1. Digital rectal examination should be included for patients with
abdominal pain (if possible)
a) fecal occult blood testing should be performed with rectal examination

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b) observe the anal opening for any obvious hemorrhoids, masses,
fissures, or external sources of bleeding
c) check anal ring sensation (anal wink)
d) failure to perform rectal examination may be associated with an increased risk
of misdiagnosis
2. Consider pelvic examination for all women of childbearing age (at the
discretion of the examiner) with appropriate STI testing; failure to
perform pelvic examination and testing may be associated with an increased
risk of misdiagnosis
G. Laboratory testing recommended with symptoms of abdominal pain
1. CBC: to rule out infection, anemia/blood loss, platelet disorder
2. Urine
a) U/A: hematuria, glucosuria, infection
b) UCG: to rule out pregnancy
3. Comprehensive metabolic profile (CMP) with liver enzymes: to rule
out liver or renal disease, electrolyte imbalance, glucose abnormality,
calcium disorder
4. Sed rate and/or CRP: marker for generalized inflammation
5. Amylase/lipase: to rule out pancreatitis
H. Radiography tests
1. Chest x-ray: to rule out pneumonia, masses
2. KUB: to evaluate for constipation, bowel obstruction, and occasionally
gallstones or kidney stones
3. Ultrasound
a) pelvis: to rule out pregnancy, ovarian cyst/tumor/torsion, fibroid
tumor
b) gallbladder U/S (or abdominal/pelvic U/S): to rule out gallstones,
masses, and GU system problems
4. CT scan (see Table 4-2)
a) abd/pelvis: to rule out masses, constipation, aneurysm, pneumonia
b) appendix: to rule out appendicitis

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 c) kidney: to rule out kidney stones
5. MRI abdomen/pelvis: to check for inflammatory bowel disease

P r a c t i c e Pe a r l s f o r B o we l C o n d i t i o n s

• Colon cancer screening guidelines according to the CDC and ACG

• The preferred colorectal cancer (CRC) prevention testing is colonoscopy

q10 yr beginning at age 50 and for African-Americans beginning at age
45; alternative testing includes flexible sigmoidoscopy q5-10 yr or CT
colonography q5 yr.
• Cancer detection testing
■ Annual fecal immunochemical test (FIT), which is considered more
sensitive than the traditional Hemoccult card for identifying occult
blood; can detect cancer up to 2 years earlier than standard FOBT.
■ Alternative testing (for those who decline colonoscopy) includes an
annual Hemoccult card or fecal DNA testing q3 yr (DNA testing is
more expensive).
• Recommendations for screening when the family history is positive for
colon cancer but evaluation for hereditary nonpolyposis colorectal
cancer (HNPCC) is not indicated:
■ Single first-degree relative diagnosed after the age of 60 years; screen as
general population
■ Single first-degree relative diagnosed at age <60 years or two first-
degree relatives diagnosed with CRC: screening includes colonoscopy
q5 yr beginning at age 40 or 10 years younger than the age of diagnosis
of the family member
• If polyps are noted on colonoscopy, then follow-up is usually q3-5 yr or
as guided by the gastroenterologist, depending on polyp biopsy.
• Constipation is a slowing of passage of stool through the colon.

• Rome III diagnostic criteria for functional constipation must include ≥2

of the following 25% of the time:
■ Straining during defecation
■ Lumpy or hard stools

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■ Sensation of incomplete evacuation
■ Sensation of anorectal obstruction/blockage
■ Manual maneuvers to facilitate defecation
■ Loose stools rarely present
■ Insufficient criteria for IBS
• Can cause hemorrhoids or anal fissures, abdominal pain, bloating, and
flatulence
• Occurs in children and adults and can be temporary or chronic
• First-line therapy for intermittent constipation
■ Increase water and fiber intake (food or supplement)
■ Exercise
■ Consider probiotics daily (either oral supplements or yogurt)
■ Stool softeners
■ Intermittent laxatives
■ Mineral oil (caution with the elderly and infants: associated with aspiration
pneumonia and can cause stool leakage)
• Constipation treatments
■ Review the patient’s medications for the cause of constipation (e.g.,
narcotics, anticholinergics, laxatives).
■ Home-prepared bulking/motility therapy for chronic constipation
• warm together 60 ml prune juice and 30 ml milk of magnesia (MOM)
and drink while warm
• PBA: mix together 1 cup prune juice, 1 tbsp unprocessed bran, and
applesauce to the desired consistency; start with 30 ml qd with
breakfast and if necessary increase weekly to a total of 90 ml tid
■ OTC medications for chronic constipation
• stool softeners: docusate sodium (Colace) up to 2 caps bid (these will
soften stools but do not usually increase peristalsis)
• bulk-forming laxative: psyllium 3.5 g 1 to 3 times qd and adjust for
stooling; bran 20 g qd

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• inulin is soluble, prebiotic, and aids in bowel function; available as a
powder and chewable or gummy bites; can worsen constipation
without adequate water ingestion. Dosing:
• children aged 6 to 12 years: 1 gummy daily (1.5 g) up to 3 a day
• adults (aged >13 years): 2 gummies (3 g) qd up to 6 a day
• stimulant laxative
• senna (either alone or with docusate sodium) qd or qod; senna has a
laxative effect and some stool-softening effect
• bisacodyl qd or q2-3d; can be taken orally or via rectal suppository
• cascara sagrada 30 ml (herbal product) use as needed for relief of
acute/chronic constipation (not usually a daily regimen); can be mixed
with MOM
• osmotic laxative
• polyethelene glycol 3350 (Miralax, Glycolax) qd; may take for up to 3
days to see the effects; may cause bloating and cramping
• lactulose 15 ml bid (start once qd); children 1 ml/kg 1 to 2 times a day
• gummy bears qd for children (sorbitol increases motility); start with 1
to 2 gummy bears and can increase as needed
• saline laxative for obstipation: magnesium citrate (adult use only)
• works within 3 hours
• may cause electrolyte imbalance
■ Water intake should be 2 to 3 L/day (unless contraindicated).
■ Monitor for worsening constipation, especially if the patient does not
drink adequate water.
■ Prescription medications for chronic constipation
• lubiprostone (Amitiza) 25 mcg bid for chronic idiopathic constipation
or 8 mcg bid for IBS constipation
• linaclotide (Linzess) 290 mcg qd for constipation related to IBD and 145
mcg qd for idiopathic constipation; give before the first meal of the day
• Hemorrhoid pain can be reduced with a compounded product of NTG ointment 2% mixed
with petroleum jelly in a 1:1 ratio, which is then mixed with hydrocortisone 1% OTC cream
in a 1:1 ratio.

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• Can apply 3 to 4 times qd
■ Wear gloves to apply (to prevent H/A).
■ Can cause H/A and hypotension if too much is used too often

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Upper abdominal problems
Gastroesophageal reflux disease (GERD)

I. Definition: reflux into the esophagus because of relaxation of the lower esophageal sphincter
(LES)

A. Common problem in all ages and can be a chronic condition that is

likely to relapse; can occur in families, especially with a history of
gastric cancer
B. Most concerning if new-onset dyspepsia occurs at >55 years of age;
consider cancer or PUD
C. Chronic erosive esophagitis is a complication of GERD, which can
lead to bleeding, anemia, scarring, and increased risk of Barrett’s
esophagus
D. Functional heartburn has similar pain as GERD but no symptom relief
with PPIs. Affected individuals are considered to be hypersensitive to
gastric acid and may need higher doses of PPIs bid or trial of tricyclic
antidepressants (TCAs) or SSRI.
II. Major risk factors

A. Obesity
B. Hiatal hernia
C. Cigarette smoking, alcohol use/abuse
D. Premature birth in infants
III. Typical signs and symptoms

A. Metallic acid taste in the mouth (acid brash), belching, and

regurgitation of fluids or foods that usually occurs about 1 hour after
eating a large meal and worsens by lying down or bending forward
B. Anterior chest pain with burning sensation that radiates to the neck
C. Pain decreases with antacids
IV. Atypical signs and symptoms

A. Chronic nonproductive cough and/or wheezing

B. Sore throat, hoarseness unrelieved with OTC antihistamines or

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 Tylenol
C. Frequent throat clearing and globus (sensation of something in the
throat)
D. Frequent OM in children
E. Noncardiac chest pain
F. Poor dentition with loss of or erosion of enamel
V. Causes of worsening symptoms (Box 10-1)
VI. Causes of aggravating reflux (Box 10-2)
VII. Not-to-be-missed signs and symptoms related to more significant diagnosis

A. Anorexia; unintentional weight loss

B. Blood in stools or emesis
C. Dysphagia or painful swallowing
D. Chronic cough or change in sputum production: consider pulmonary
disease/disorders
E. Chronic unremitting reflux, hoarseness, and swallowing problems:
consider Barrett’s esophagus (highest risk in obese white males aged
>50 years)
VIII. Diagnostic tests

A. “Clinical history” is a good indicator of disease

B. CBC (should be normal)
C. Refer for EGD
D. Helicobacter pylori testing if unresponsive to therapy or if the
symptoms are suggestive of infection
IX. Treatment

A. If there are no alarming symptoms and the clinical history indicates

that GERD is the probable cause: initiate lifestyle modifications first to
help decrease symptoms and prevent recurrence
1. Do not eat meals or drink carbonated beverages 3 hours before
bedtime
2. Decrease the amount of fried, fatty, and spicy foods to decrease gastric
acid production

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3. Raise the head of the bed using 4-to 6-inch blocks, especially if
nocturnal symptoms are present
4. Decrease weight if indicated
5. Decrease or eliminate the use of caffeine, nicotine, and alcohol
6. Avoid foods that relax the LES (see Box 10-1)
7. Decrease or eliminate NSAID use
B. Drug therapy (also see Table 10-2, H2 Blockers/PPIs)
1. Initial therapy
a) initially, use antacids whenever symptoms are present after meals
b) if symptoms are predictable, use antacids 1 hour before meals, after
meals, and at hs
c) use OTC H2 blockers before the morning meal and at hs (hs dosing is
useful with nocturnal reflux)
2. If symptoms are intense and predictable
a) prescription-strength H2 blockers and PPIs can be used 12 hours apart;
PPIs taken bid can be effective if qd dosing does not give 24-hour relief
b) antacids and H2 blockers can be used on the same day but not at the
same time
c) use PPIs for 8 weeks and then stop; if symptoms recur, restart at a
lower dose indefinitely but be aware that long-term dosing with PPIs
can lead to increased hip fracture risk in postmenopausal women,
increased risk of Clostridium difficile infection and B12 deficiency, and
can alter calcium balance and interfere with cardiac conduction defects
d) try intermittent dosing or tapering off H2 blockers or PPIs after 8
weeks; decrease medications slowly to avoid acid rebound effect
e) increased-dose H2 blockers may not relieve symptoms better (no
increased dose-response curve noted)
C. Referral to a gastroenterologist
1. If no response to therapy
2. If continuous chronic treatment is needed because of Barrett’s
syndrome

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 3. If persistent reflux symptoms are unrelieved with medications after 4
weeks of full-dose therapy with PPIs and H2 blockers
Table 10-1
Differential Diagnoses of Abdominal Pain in Young Patients

Infant to 12 mos 2-5 yrs 6 -11 yrs 12 yrs to Adult

Infantile colic Gastroenteritis Gastroenteritis Appendicitis
Gastroenteritis Appendicitis Appendicitis Gastroenteritis
Constipation Volvulus Constipation Cholecystitis
Intussusception Constipation Mesenteric lymphadenitis Pancreatitis
Hirschsprung’s disease UTI Functional pain Constipation
Trauma Trauma, drugs, toxins UTI Dysmenorrhea
Testicular torsion Pharyngitis Trauma, drugs, toxins Mittelschmerz
UTI Mesenteric lymphadenitis Pharyngitis PID
Incarcerated hernia Diabetic ketoacidosis Pneumonia Pregnancy
Necrotizing enterocolitis Henoch-Schönlein purpura Sickle cell crisis Ovarian torsion
Milk protein allergy Testicular torsion
Diabetic ketoacidosis
IBD, celiac disease

Table 10-2
H2 Blockers and Proton Pump Inhibitors

Medication Dosage
H2 Blockers
Ranitidine 150 mg bid or 300 mg hs
Cimetidine** 400 mg bid or 800 mg hs
Nizatidine 150 mg bid or 300 mg hs
Famotidine 20 mg bid or 40 mg hs
Famotidine/calcium carbonate/magnesium 1 tab q12h prn heartburn
hydroxide
Proton Pump Inhibitors (PPIs)***
Omeprazole (OTC, Rx) 20-40 mg qd/bid
Lansoprazole (OTC, Rx) 15-30 mg qd
Rabeprazole 20 mg qd
Esomeprazole 20-40 mg qd
Pantoprazole 40 mg qd
Omeprazole + sodium bicarbonate (Zegerid)* 20 mg qd for 4 wks and give 1 h before a
meal

• Zegerid dosing is based on omeprazole dose not on bicarbonate dose.

• Two 20-mg caps or powder packet is not bioequivalent to one 40-mg dose.
• Immediate-release powder can be used for patients who cannot swallow pills (i.e., children

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and patients with feeding tubes).
• Children (1 to 16 years of age), 10 to 20 kg: 10 mg qd; >20 kg: 20 mg qd
• Zegerid is both OTC and Rx (Rx dosing 20 to 60 mg strength, OTC 20 mg).
• Zegerid should be taken at least 1 hour before a meal.
*Special
considerations for Zegerid
**Cimetidine
can cause confusion in elderly people; always check medications being used.
***PPIs
should be taken half an hour before a meal for peak effect.

Box 10-1

Factors That Worsen Symptoms by Relaxing LES

Foods:

Chocolate
Peppermint
High-fat foods
Medicines:

Theophylline
Anticholinergic medications
Progesterone
Calcium channel blockers
Alpha adrenergic agents
Diazepam

Box 10-2

F a c t o r s T h a t A g g r a va t e R e f l u x S y m p t o m s
Foods:

Citrus fruits
Spicy foods
Tomatoes
Coffee

Medicines:

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 Tetracycline
Quinidine
Potassium
Iron salts
NSAIDs and ASA
Bisphosphonates

Peptic ulcer disease (PUD)

I. Definition: disruption of the mucosal lining of the stomach, duodenum, or both that results in
an ulcer

A. Commonly associated with H. pylori disease (either current or past)

and chronic NSAID or steroid use
B. Risk factors include smoking, alcohol use, and advanced age
C. Common between 40 to 60 years of age but can occur in children
under stressful conditions
II. Signs and symptoms

A. Pain
1. Chronic recurrent upper abdominal pain (epigastric or retrosternal)
that is burning, gnawing, aching, and described as “hunger pains”
2. With duodenal ulcers: pain may occur on empty stomach and is
usually relieved with food, antacids, or liquids such as milk or ice
cream
3. With gastric ulcers: pain occurs after eating and is present until the
stomach has emptied; is usually absent with fasting
4. Nocturnal pain may occur but this is usually related to GERD
5. Epigastric pain with palpation and guarding is common
B. N/V, constipation may occur
C. Anorexia, weight loss, and feeding difficulties in young children
III. Complications

A. Acute perforation with severe abdominal pain and peritoneal signs

B. Hemorrhage, shock, hypotension
IV. Not-to-be-missed signs

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 A. Weight loss; recurrent or intractable vomiting
B. GI bleeding; anemia
C. Dysphagia
D. New-onset dyspepsia, especially with age >55 years
V. Diagnostic testing

A. CBC (may show mild microcytic anemia), stool FOBT (may be

positive for blood)
B. H. pylori testing (should be negative)
C. Consider referral for endoscopy
VI. Treatment

A. Nonpharmacologic therapy
1. Review all current medications including OTC and herbal products;
stop all NSAIDs and decrease steroid therapy to the lowest possible
dose
2. There is a high risk of recurrence, especially if lifestyle changes are not
instituted; if the ulcer recurs, can use half-dose acute phase
medications indefinitely
3. Stop smoking and alcohol intake
4. Diet should be nutritious with frequent, small meals; no spicy, fried, or
fatty foods or foods that irritate the stomach lining
B. Pharmacologic therapy
1. Misoprostol therapy at 100 to 200 µg qid with food is useful for
preventing NSAID-induced ulcers in patients on long-term NSAID
therapy
2. Probiotic supplements may speed healing
3. Vitamin C at 500 mg 2 to 3 times qd may help healing (no data
confirmation but is not harmful)
4. Treat H. pylori if present (see H. Pylori, IV in this chapter)
C. If H. pylori testing is negative, begin symptomatic treatment for 4 to 6
weeks
1. Antacids 2 to 4 tbsp 1 hour before and 2 hours after meals/medications

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 and at hs (magnesium antacids tend to cause diarrhea; aluminum
antacids tend to cause constipation; use combination products to
counteract side effects)
2. H2 blockers (see Table 10-2) given in split dose or at hs
3. PPIs (see Table 10-2) are most effective if given 30 minutes before a
meal
4. Sucralfate 1 g 30 to 60 minutes before meals and at hs (especially
useful with NSAID-induced ulcer)
D. Surgical referral may be needed for patients with nonhealing ulcers
who do not respond to medical therapy

Helicobacter pylori-induced gastritis

I. Definition: a primary infection of the protective lining of the stomach caused by Helicobacter
bacteria by-product called urease, which makes the stomach lining more vulnerable to digestive
enzymes

A. Found in ∼50% of the population; usually acquired in childhood

B. Most common route of entry is the oral or fecal-oral route
C. Infection may last years because of the difficulty in “eradicating”
bacteria
D. Associated with cancer in the stomach and is the most common cause
of PUD
II. Signs and symptoms

A. Similar to PUD but may not be as intense

B. Dyspepsia, hunger in the morning, and possible halitosis
C. Bloating
D. Increased belching, burping, and fullness after a small meal
III. Diagnostic testing

A. CBC (may have slight microcytic anemia), FOBT (may be positive)

B. H. pylori testing (will be positive)
C. Endoscopy is indicated if poor response to medical therapy
IV. Treatment with the goal of symptom relief

Doses Efficacy

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 10-Day Treatments
Amoxicillin 1 g bid 70%-85% effective
Clarithromycin 500 mg bid
PPI of choice (see Table 10-2)

Metronidazole 500 mg bid 70%-85% effective

Clarithromycin 500 mg bid
PPI of choice (see Table 10-2)

Bismuth subsalicylate 525 mg qid 75%-90% effective

Metronidazole 250 mg qid
Tetracycline 500 mg qid
PPI of choice (see Table 10-2)

14-Day Treatments
Prevpac (lansoprazole/amoxicillin/clarithromycin) 1 dose bid 70%-85% effective

Helidac (bismuth subsalicylate/metronidazole/tetracycline) 1 dose qid 75%-90% effective

A. Retreatment should be considered if previously positive for H. pylori

and symptoms return
V. Referral to a gastroenterologist for endoscopy if symptoms are not relieved with therapy

P r a c t i c e Pe a r l s f o r H . p yl o r i f o r G E R D M e d i c a t i o n s

• Foods containing flavonoids such as apples, cranberries, garlic, and tea may inhibit the
growth of H. pylori.
• Bismuth causes stools to turn black and the patient’s tongue may become black on the dorsal
side; both should resolve after treatment.
• Avoid drinking alcohol while taking metronidazole because of vasomotor reactions (e.g.,
vomiting, flushing, and sweating) that should resolve after treatment.
• Metronidazole and clarithromycin may cause a metallic taste in the mouth that should
resolve after treatment. Note the rate of resistance in your area, may not be first-line
therapy.

Cholecystitis

I. Definition: acute or chronic inflammation of the gall bladder usually caused by gallstones or
poor gall bladder function

A. Most commonly occurs in women of childbearing age and those in the

sixth decade of life
B. Women on OCs are at a higher risk

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 C. More common in obese people
D. Native Americans have a 75% increased risk of gallstones
E. People experiencing rapid weight loss are at a higher risk of
developing gallstones
II. Signs and symptoms

A. History of a fatty meal before starting of pain; may have N/V after a
meal
B. Heartburn and dyspepsia
C. Pain and tenderness in the RUQ or epigastrium with/without
radiation to the infrascapular region, mainly on the right side
D. Palpation in the RUQ elicits marked tenderness with deep inspiration
(Murphy’s sign)
E. Guarding
III. Diagnostics

A. CBC (may show leukocytosis with left shift)

B. Amylase and alkaline phosphatase (may be elevated), total bilirubin
(may be mildly or markedly elevated)
C. Consider ECG to rule out cardiac origin
D. Consider CXR to rule out pneumonia
E. U/S gallbladder; if negative and symptoms continue, consider HIDA
scan to test the function of the gallbladder (U/S is the first test, because
presence of gallstones must be excluded before performing HIDA
owing to the potential rupture of the gallbladder if the stone is
occluding the cystic duct)
IV. Treatment: refer to a surgeon if gallbladder tests are positive for stones or dysfunction or if
symptoms continue after adequate medical therapy

Acute gastroenteritis

I. Description: sudden onset of diarrhea accompanied by nausea and vomiting

A. May be caused by virus, bacteria, or parasites

B. Can last up to 10 days but is primarily a self-limiting illness in
immunocompetent people

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II. Signs and symptoms

A. Dehydration is the most important sign to be aware of in infants, children,

and the elderly and must be treated; the level of severity will determine
treatment (see Table 17-1, Signs of Dehydration)
B. Usually acute-onset N/V with flatulence and explosive diarrhea
C. Often associated with myalgia, headache, malaise
D. Diffuse tenderness of the abdomen with hyperactive bowel sounds
III. Diagnostic testing

A. CBC, BMP (basic metabolic profile)

B. If diarrhea continues beyond 3 to 5 days, may consider stool cultures
and stools for O&P (some laboratories have specific requirements for
testing, contact your lab for special ordering needs)
IV. Treatment

A. Refer immediately if obvious dehydration requiring multiple IV fluids or

resuscitative therapies and/or positive neurological signs are present along
with abdominal pain with N/V and rigidity
B. Monitor closely the first 48 hours for changes in the hydration status
and instruct caregivers on symptoms of worsening condition,
especially if the patient is very young or elderly
C. Bed rest and recheck in office in 24 hours
D. IV therapy in office with normal saline (if available) reduces the risk
for dehydration
E. Home oral rehydration therapy (Table 10-3) should be initiated as
soon as possible
F. Start zinc supplements for 1 month: 20 mg qd if >6 months old, 10 mg
qd if <6 months old
G. Start probiotics qd for 1 month
H. Can use ondansetron (Zofran) 4 to 8 mg q8-12h (based on age/weight)
for nausea
I. Antidiarrheals are not recommended; can use bulking agents (fiber
products) daily to help bulk stools
J. Diarrhea may last for 10 days (or longer in postinfectious motility

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 disorders) but should have decreasing symptoms qd
Table 10-3
Oral Rehydration Solution Mixtures

Special
Mixture Name Mixture Administration
Considerations
Pedialyte 3:1 sugar/salt ratio Give frequent sips, not gulps, Do not use red drinks
Pedialyte Advanced q30-60 min Start at first symptoms of
Care (contains diarrhea to maintain
prebiotics) hydration
Continue breast-feeding

Oral rehydration Glucose:salt:potassium 1 packet in 1 L water There are several similar

salts concentration (∼3:2:1 Give in small amounts q30-60 min commercial products on
ratio) the market
Start at first symptoms of
diarrhea
Continue breast-feeding

Drip Drop Dissolve 1 packet in 500 ml water Use with caution in

Do not mix with other solutions anyone on a salt-
restricted diet
Give in small amounts at
a time
Caution under 1 year of
age

Oral rehydration Glucose:salt water Mix 6 tsp sugar + ½ tsp salt to 1 L of Water should be boiled
solution (made at solution (3:0.5% ratio) water (measure carefully*) for 15 min or use distilled
home) water
Mixture should be cooled
before administering
Same administration
instructions as above
Do not use artificial
flavoring
Continue breast-feeding

Cereal-based oral ½-1 cup precooked baby rice cereal or Should be thick enough
rehydration 1 ½ tsp of granulated sugar + 2 cups to drink
therapy water + ½ tsp salt Give often by spoonfuls
Give even if vomiting
Can put in mashed
banana or other
nonsweetened fruit
Mix with a cold product
or serve cold; may be
more palatable
Discard any remaining
solution after 24 h and
make new

*
Watered-down formula does not provide enough calories. Foods high in simple sugars might worsen diarrhea.

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Pancreatitis

I. Definition: inflammation of the pancreas, which produces enzymes for digestion and insulin
for control of blood sugar. When the pancreas is inflamed, there is a leakage of pancreatic
enzymes into the surrounding tissues.

A. Usually caused by chronic ingestion of alcohol

B. Can be caused by gallstones that block the duct of the pancreas or
cancer
II. Signs and symptoms

A. Mild-to-severe, chronic sharp pain in the upper abdomen that may

radiate to the back or chest
B. N/V, fever
C. Signs of intraabdominal bleeding with ecchymosis in the flanks or
periumbilical region (e.g., Grey-Turner’s sign or Cullen’s sign,
respectively)
D. Weight loss (unexplained)
E. Hypotensive signs: tachycardia, sweating, tachypnea
III. Diagnostic testing

A. Diagnostic criteria
1. Characteristic abdominal pain
2. Amylase and lipase >2 to 3 times the normal
3. Imaging findings consistent with pancreatitis
B. CBC (elevated WBC), amylase and lipase (elevated), complete
chemistry panel (low calcium and magnesium); monitor amylase and
lipase every 3 months as needed until stable, then q1 yr or as needed
depending on the patient’s history
C. U/S pancreas or CT upper abdomen (see Table 4-2): usually definitive
test
IV. Treatment

A. Referral to a hospital for severe pain and suspected pancreatitis for

further evaluation, fluids, pain management, and rest
1. A low-fat diet is recommended for chronic pancreatitis; patients
should limit foods high in trans-fats or trans-fat substitutes (e.g.,

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 cookies, crackers, cakes, and donuts)
2. Encourage foods high in antioxidants, such as green leafy vegetables,
cold-water fish, beans, berries, tomatoes, and foods high in vitamin B
and iron
3. Decrease or eliminate alcohol, caffeine, and tobacco
4. Maintain normal or low levels of lipids, especially triglycerides
B. Supplements for deficiencies related to pancreatitis
1. Multivitamin, omega-3 fatty acids
2. Co-Q10 100 to 200 mg at hs
3. Vitamin C 1 to 6 g qd (lower dose if diarrhea occurs)
4. Probiotic supplement qd
C. Suggest counseling or psychological assistance for abusive habits

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Lower abdominal problems
Irritable bowel syndrome (IBS)

I. Definition: Rome III criteria for diagnosis of IBS: symptoms present for at least 3 days in the
past 3 months (with symptom onset at least 6 months previously), with ≥2 of the following
features:

A. Pain is relieved with stooling

B. Onset of pain associated with change in frequency of stools
C. Onset of pain associated with change in consistency of stools
D. IBS affects motility of the colon and does not normally cause damage
to the colon or increased risk of cancer
E. Most often seen in people with depression, panic, anxiety, and
fibromyalgia
F. Most concerning if new onset of symptoms occurs in people aged >50
years and/or those with a family history of inflammatory bowel
disease or cancer
II. Signs and symptoms (usually do not disturb sleep)

A. Abdominal distention, gas, and bloating, with crampy lower

abdominal pain
B. Pain
1. Associated with meals
2. Associated with menstrual cycles
3. Worsens with stress
4. Relieved with passage of flatus or stool
C. Diarrhea or constipation with small-volume stools with clear-white
mucus
D. No bleeding in stools and no weight loss noted even with significant
symptoms
E. Rectal examination is usually normal
F. Not to be missed

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 1. Fever, chills, night sweats, and nocturnal symptoms
2. Weight loss
3. Melana, hematochezia; anemia
III. Diagnostic testing may not yield conclusive data and testing is used to rule out more severe
illnesses

A. CBC, comprehensive chemistry panel, TSH, ESR, CRP

B. Stool samples for culture and O&P
C. Consider referral to a gastroenterologist: for possible evaluation of
celiac disease with small intestine biopsy; EGD and/or colonoscopy
D. If stool is greasy, check for chronic pancreatitis with abdominal CT
(see Table 4-2)
IV. Treatment with lifestyle changes

A. Exercise, including vigorous exercise 3 to 5 times per week

B. Fiber and laxatives may or may not be effective
C. Dietary changes on a trial basis to include the following:
1. Lactose-free foods/fluids
2. Avoid flatulence-producing foods (e.g., beans, brussels sprouts,
cabbage, grapes, raisins, wine, beer)
3. Avoid eating large meals as well as fried, spicy, or fatty foods
D. Increase water intake
E. Stress reduction techniques
V. Pharmacologic therapy

A. Diarrhea-predominant symptoms
1. Loperamide (Imodium) 2 mg initially after each stool up to 16 mg/day
prn severe diarrhea
2. Probiotics daily (lactobacillus, bifidobacterium)
3. SSRIs (any type)
4. PPIs or H2 blockers (see Table 10-2) for chronic diarrhea and urgency
after meals; should see a decrease in symptoms in 3 to 4 days
B. Constipation-predominant symptoms

355
 1. Lubiprostone (Amitiza) 8 mcg bid (adults only) or
2. Linaclotide (Linzess) 290 mcg qd (adults only)
3. Peppermint oil may relax smooth muscle
4. Probiotics daily
C. Cramping IBS pain
1. Dicyclomine HCl 20 to 40 mg qid prn or
2. Hyoscyamine sulfate (Levbid) 0.375 mg q12h prn or
3. Clidinium/chlordiazepoxide (Librax) 1 to 2 caps ac and hs prn

Diverticulitis

I. Definition: inflammation and/or infection of a saclike out-pouching of the bowel wall

(diverticulosis); microperforation is a possible complication of diverticulosis from trapped food.
The perforation is walled off and becomes an abscess.

A. Usually involves only one diverticulum

B. Can progress to a life-threatening illness secondary to an abscess, free
perforation into the peritoneum, and fistula formation
II. Signs and symptoms

A. Recurrent, intermittent LLQ pain and tenderness with increased

flatulence; changes in bowel habits can occur
B. Acute LLQ pain
C. Fever, chills, N/V/D (or constipation)
D. Leukocytosis
E. Mass in the LLQ
F. Decreased bowel sounds
G. DRE may reproduce pain in the LLQ; stool may be positive for occult
blood
III. Diagnostic testing

A. CBC (usually shows leukocytosis), urinalysis (should be normal)

B. Abdominal ultrasound (may demonstrate colon wall thickness and
fluid collection, which could be abscess formation
C. Abdominal CT is the diagnostic test of choice (see Table 4-2)

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 D. Refer for colonoscopy to identify diverticula (this is usually not
performed acutely)
IV. Treatment of acute diverticulitis: transfer to ED if signs are consistent with perforation of the
colon
V. Treatment of nonsurgical/uncomplicated diverticulitis

A. Bowel rest with a low-fiber diet; increase fluid intake to maintain

hydration, and slowly progress to bland, soft foods over a period of
about 10 days
B. Avoid laxatives, enemas, and bulk additives such as psyllium in the
acute phase
C. Antibiotic treatment for 7 to 10 days
1. Metronidazole 250 to 500 mg q6h plus
2. Bactrim DS 1 tab bid or
3. Ciprofloxin 500 to 750 mg bid or
4. Levofloxacin 750 mg qd or
5. Cefdinir 300 mg q12h or
6. Moxifloxacin 400 mg qd
7. Drugs no longer recommended because of increased resistance:
amoxicillin/clavulanate, clindamycin, cefotetan
D. Follow-up treatment of diverticulitis
1. High-fiber diet
2. Stool softeners
3. Decrease intake of nondigestible foods such as corn, popcorn, and nuts
(debatable at this time)
4. Follow-up in office 4 weeks after resolution; refer to a
gastroenterologist for colonoscopy

Appendicitis

I. Definition: inflammation and/or rupture of the appendix

II. Signs and symptoms

A. Anorexia

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 B. Low-grade fever (possibly)
C. Stooped appearance when walking
D. Presence of one or more of these signs increases likelihood
1. Pain worsens with movement, coughing, and deep breathing and is
located in the RLQ
2. Pain migration from the periumbilical region to RLQ
3. Pain noted before vomiting
4. Positive psoas sign (see Abdominal Pain, V, E in this chapter)
5. Positive Markle’s sign (see Abdominal Pain, V, E in this chapter) is a
good predictor of peritoneal irritation with appendicitis
III. Diagnostic testing

A. CBC (may show leukocytosis), UA (usually normal)

B. Flat and erect abdominal x-ray (may show fecalith)
C. Abdominal U/S for children (less invasive but the appendix may not
be visualized)
D. CT abdomen for appendicitis (see Table 4-2)
IV. Treatment: if any tests are positive or if the symptoms continue, refer to a surgeon or ED for
further follow-up

Colon cancer

I. Increased risk

A. ≥40 years of age

B. FH of colon cancer
C. Adenomatous polyps on past colonoscopy
D. Inflammatory bowel disease
E. Sedentary lifestyle
F. Fiber-deficient diet
II. Signs and symptoms

A. Right side colon involvement

1. May be asymptomatic until the tumor causes obstruction

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 2. Unintentional weight loss
3. Anemia; positive FOBT
4. Crampy, colicky, intermittent abdominal pain
B. Left side colon involvement
1. Diarrhea or constipation and fullness after defecation
2. Shape of stool changes
3. Anemia; bright red rectal bleeding mixed with normal stool
4. Generalized lower abdominal pain
5. Unintentional weight loss
C. Sigmoid/rectal colon involvement
1. Obvious rectal bleeding or bleeding mass at anal opening
2. Mucoid drainage from the anus
3. Pain with defecation
III. Diagnostic testing

A. CBC (may show anemia)

B. Stool positive for occult blood
C. Abdominal CT may show mass (see Table 4-2)
D. Refer to a gastroenterologist for colonoscopy and biopsy of the lesion
IV. Treatment: referral to a surgeon for definitive care

Celiac sprue disease (gluten intolerance enteropathy)

I. Definition: T-cell-mediated autoimmune inflammatory disease of the small intestine that can
involve multiple other organ systems

A. Occurs only after exposure to gluten in genetically sensitive people

(gluten is a protein found in wheat, rye, barley, and possibly oats)
B. Causes damage to the absorptive surface of the intestinal mucosa,
resulting in poor digestion of foods and malabsorption of nutrients,
with failure to thrive and diarrhea (classic form)
C. Can affect any age after solid foods are introduced
II. Signs and symptoms

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 A. Diarrhea
1. Watery or semi-formed stools with change in color and consistency
with foul odor
2. Steatorrhea
B. Flatulence and borborygmus due to excessive release of gas produced
by bacterial flora; may be excessive or even explosive
C. Weight loss; in children, will see failure to thrive and growth
retardation
D. Weakness due to poor general nutrition
E. Anemia and hypokalemia
F. Abdominal bloating and cramps are common
G. Extraintestinal symptoms: neuropathy, osteoporosis, dermatitis
herpetiformis
III. Diagnostic testing

A. CBC, CMP, Vitamin D, Fe, and zinc

B. Tissue transglutaminase IgA and total IgA
C. Stool samples for fecal fat
IV. Treatment

A. Referral to a gastroenterologist for further testing and evaluation

B. If celiac disease (gluten allergy) is confirmed, education regarding
avoidance of all gluten-containing grain products

Inflammatory bowel diseases (IBD)

Crohn’s disease (regional enteritis)

I. Definition: chronic recurring immune response and inflammation that may involve
discontinuous segments of the GI tract from the mouth to the anus

A. Occurs at any age

B. Increased risk of colon cancer
II. Signs and symptoms

A. Intermittent diarrhea followed by constipation with recurrent

episodes of mucoid diarrhea

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 B. Colicky or steady abdominal pain located in the RLQ or periumbilical
region
C. Anorexia, flatulence, malaise, and weight loss
D. Perianal disease with fistula and skin tags
E. Extraintestinal manifestations may occur in musculoskeletal and
dermatologic sites about ≥10 years after diagnosis
III. Diagnostic testing

A. CBC (may show macrocytic anemia), ESR/CRP, and CMP (to monitor
albumin)
B. Positive blood in stool
C. Abdominal CT (see Table 4-2)
IV. Treatment

A. Refer to a gastroenterologist or surgeon for further management

depending on the severity of symptoms
B. Stop smoking
C. Stay up to date with immunizations (especially flu and pneumonia)
D. Nonresidue diet with high protein, vitamins, and calories; avoid raw
fruits and vegetables

Ulcerative colitis (UC)

I. Definition: inflammation that involves the colon and rectum

A. Primarily in young adults

B. Increased risk of colon cancer
II. Signs and symptoms

A. Frequent episodes of bloody mucus and pus from the rectum

B. Diarrhea can occur without warning
C. Cramping abdominal pain is usually mild
D. Anorexia, malaise, weight loss, and fatigue
E. Rectal tenesmus
F. Intolerance of dairy products periodically; consider avoiding during
acute flares

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 G. Occasional skin tags and aphthous ulcers
III. Diagnostic testing

A. CBC (may show microcytic anemia), CMP, ESR/CRP (usually

elevated)
B. Stools positive for blood
C. Abdominal/pelvic CT (see Table 4-2)
IV. Treatment

A. Refer to a gastroenterologist for management

B. Stop smoking
C. Avoid milk products with acute flares, increase intake of
calcium/vitamin D supplements

Diarrhea

I. Diarrhea has many causes; some will resolve without treatment and some will need treatment
because of the infectious nature or damage to the colon

A. Diagnostic testing
1. Diarrhea lasting >1 week will need to be evaluated by stool testing for
the following:
a) ova and parasites (O&P), culture and sensitivity (C&S) for bacteria
b) Clostridium difficile infection, especially with recent antibiotic use
c) blood
2. Fecal fat (fat malabsorption syndrome)
3. Fecal alpha-2 antitrypsin (protein malabsorption)
B. Radiographs
1. Abdominal films (flat and upright)
2. UGI with small bowel follow-through
3. Barium enema
C. Other laboratory tests
1. CBC (should be normal), ESR/CRP (may be elevated)
2. Comprehensive chemistry profile with liver function, amylase and

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 lipase, and protein/albumin
D. Refer for colonoscopy if persists beyond 2 weeks and is difficult to
control
II. Staphlococcus aureus diarrhea

A. Definition: usually occurs from improperly handled food and unclean

food handlers (bacterial infection)
1. Transmission route: fecal-oral, with onset in 1 to 6 hours after exposure
2. Resolves in about 1 to 2 days
B. Signs and symptoms
1. Intermittent watery diarrhea without blood, mucus, or foul odor
2. No fever
3. Positive abdominal pain and N/V
C. Treatment
1. Supportive care and rehydration (see Table 10-3)
2. Rest
3. Antidiarrheals may not improve outcomes
III. Salmonella spp.

A. Definition: bacterial infection occurs from contaminated water/food

1. Transmission routes: fecal-oral and occasionally through aquatic pets
2. Onset occurs 1 to 3 days after exposure
3. Resolves in about 4 to 7 days
B. Signs and symptoms
1. Diarrhea with occasional blood and mucus and foul odor
2. Fever
3. Abdominal cramps with vomiting at onset of illness
C. Treatment
1. Supportive care and oral rehydration at onset of illness (see Table 10-3)
2. Antibiotics not indicated except for infants and elderly with life-
threatening symptoms: may use

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 a) TMP/SMX 10 mg/kg/day bid for 5 days or
b) ciprofloxacin 250 to 500 mg bid for 7 to 10 days or
c) ampicillin 50 mg/kg/day ÷ qid for 7 days
3. Report to health department
IV. Shigella spp.

A. Definition: bacterial infection caused by contaminated foods and

water
1. Transmission routes: person-person, fecal-oral, and water
2. Onset within 24 to 48 hours after exposure
3. Resolves in about 5 to 7 days
B. Signs and symptoms
1. Watery diarrhea that might contain blood or mucus
2. Positive fever
3. Abdominal cramps
C. Treatment
1. Supportive care with oral rehydration (see Table 10-3)
2. Antibiotics
a) TMP/SMX 10 mg/kg/day bid for 5 days or
b) ciprofloxacin 250 to 500 mg bid for 7 to 10 days
3. Report to health department
V. Campylobacter jejuni

A. Definition: bacterial infection caused by raw or undercooked poultry,

unpasteurized milk, and contaminated water
1. Transmission routes: fecal-oral, pets, and person-person
2. Onset occurs 2 to 5 days after exposure
3. Resolves in about 2 to 10 days
B. Signs and symptoms
1. Vomiting
2. Watery diarrhea with blood and mucus but no foul odor

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 3. Fever
4. Abdominal cramps
C. Treatment
1. Supportive care with oral rehydration (see Table 10-3)
2. For severe cases, use the following:
a) erythromycin 50 mg/kg/day ÷ tid for 5 days or
b) azithromycin (Zpak) for 5 days
D. Guillain-Barre syndrome has been associated with Campylobacter
illness
VI. Clostridium botulinum

A. Definition: bacterial infection caused by contaminated food, home-

canned foods, honey, foods kept warm for too long
1. Transmission route: fecal-oral
2. Onset occurs 12 to 72 hours after exposure
3. Resolves after treatment
B. Signs and symptoms
1. Vomiting, diarrhea
2. Blurred vision, diplopia
3. Dysphagia
4. Descending muscle weakness
C. Treatment
1. Report to health department
2. Emergent referral to ED
VII. Norwalk-like virus and rotavirus

A. Definition: viral illnesses caused by foods touched by infected

workers (e.g., daycares, cruise ships)
1. Transmission routes: fecal-oral and person-person
2. Onset occurs about 1 to 3 days after exposure
3. Resolves in 3 to 5 days

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 B. Signs and symptoms
1. Vomiting and watery diarrhea
2. Low-grade fever
3. Dehydration
4. May have temporary lactose intolerance
C. Treatment
1. Supportive care with oral rehydration (see Table 10-3) as soon as
symptoms occur; refer to ED if unable to keep fluids down
2. No antibiotics
3. Probiotics daily
4. Antiemetic consideration: ondansetron 4 to 8 mg q8-12h depending on
age
VIII. Giardia lamblia

A. Definition: protozoan illness caused by contaminated water,

contaminated food, and food touched by infected workers
1. Transmission routes: water, fecal-oral, and swimming in contaminated
water
2. Onset occurs in about 1 to 2 weeks
3. Resolves after treatment
B. Signs and symptoms
1. Stomach cramps and gas
2. Diarrhea without blood or mucus but with foul odor
3. Weight loss
4. Positive emesis
5. No fever
C. Treatment
1. Oral rehydration therapy (see Table 10-3) as soon as symptoms start
2. Antibiotics
a) metronidazole for 5 to 7 days

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 (1) adult: 250 mg tid
(2) children: 15 mg/kg/day ÷ q8h or
b) tinidazole
(1) adults: 2 g once
(2) children (>3 years): 50 mg/kg once or
c) nitazoxanide (Alinia) q12h for 3 days
(1) adult: 500 mg
(2) children: 1 to 3 years: 100 mg/5 ml, 1 tsp; 4 to 10 years: 2 tsp
3. Report to health department
IX. Traveler’s diarrhea (TD)

A. Definition: usually self-limiting bacterial illness

1. Most common illness affecting international travelers
2. Transmission: contaminated food/water (most common with E. coli)
3. Usually occurs in the first week of travel but may occur as late as after
arrival at home
4. Most cases resolve in 1 to 7 days without treatment
5. Consider treatment for high-risk people
a) young infants and elderly
b) immunocompromised people
c) presence of IBS/colon disease
d) diabetics
e) people on H2 blockers or antacids
B. Signs and symptoms
1. Profuse watery diarrhea without blood, mucus, or foul odor; usually
abrupt onset
2. Possible fever and emesis
3. Positive abdominal pain, cramping, and bloating
4. Malaise
C. General treatment

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 1. Travelers’ diarrhea does not require antibiotics unless diarrhea is
severe. Prompt symptom control is the treatment of choice.
2. Oral rehydration (see Table 10-3) at onset of illness
3. Antidiarrheal: loperamide 2 mg after loose stools (max dose 16
mg/day); can give with antibiotic therapy
4. Start bismuth subsalicylate 2 tabs or 1 oz q30 min up to 8 doses in 24
hours at the start of diarrhea; may cause black discoloration of tongue
and stools
a) bismuth subsalicylate can be used as prophylaxis: 2 tab qid or 2 oz qid
for up to 3 weeks
b) may decrease incidence of TD (avoid if allergy to ASA)
5. Antibiotic therapy for 3 days
a) cipro 250 to 500 mg bid or
b) TMP/SMX DS bid (check resistance in the area) or
c) azithromycin (Zpak)
6. If diarrhea persists for >7 days or dehydration occurs, seek medical
care
D. Prevention
1. Consume only bottled water or canned vegetables; avoid ice, salads,
and fruit (unless you peel it)
2. Beware of crowded pools, which could be a source
X. Clostridium difficile diarrhea (C. diff diarrhea)

A. Definition: diarrhea caused by broad-spectrum antibiotic use and

hospitalization; commonly seen in elderly and immunocompromised
people
1. Fourth most common nosocomial infection
2. Most common antibiotics as causative agents
a) clindamycin
b) second-and third-generation cephalosporins
c) fluoroquinolones
d) amoxicillin

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3. The person may not consider diarrhea a problem initially
B. Signs and symptoms
1. Diarrhea within 1 to 2 weeks after antibiotic use or recent
hospitalization
2. Stool is watery to semi-formed and has a foul odor with no visible
blood (at first)
3. Leukocytosis
4. Ileus is possible
5. Malaise, anorexia, and weight loss
C. Diagnostic testing
1. Stool for cytotoxin assay for C. diff and stool culture
2. CBC, U/A, CMP (if elderly or diarrhea >1 week)
D. Generalized treatment
1. Stop offending antibiotic, which may cause diarrhea to cease in 2 to 3
days and may require no further treatment
2. Evaluate for dehydration and use oral rehydration solutions (see Table
10-3)
a) may need hospitalization if significant dehydration is present and the
patient is unable to tolerate food or liquids
b) may need IV fluids initially
c) follow-up with home health referral for monitoring
3. Avoid milk and milk products, alcohol, caffeine
4. No antidiarrheals recommended
5. Strict cleaning of the house and personal items with hot water (120°F)
and good hand hygiene
E. Pharmacologic treatment
1. First episode: metronidazole (do not use metronidazole after the first
episode because of increased potential for neurotoxicity)
a) adult: 500 mg tid for 10 to 14 days
b) children: 30 mg/kg/day ÷ q6h for 10 to 14 days

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2. If the condition is severe or if metronidazole does not work in 5 to 7
days, use vancomycin (can use injectable form and give orally; can
give rectally if ileus is present)
a) adult: 125 mg qid for 10 to 14 days
b) children: 40 mg/kg/day ÷ q6h for 10 to 14 days
3. Second episode: vancomycin treatment (as above) if not used earlier
4. Third episode: pulse therapy vancomycin dosing: 125 mg qid for 14
days, then bid for 7 days, then qd for 7 days, then once q2 days for 8
days, then q3 days for 15 days
5. If symptoms continue
a) fidaxomicin (Dificid) 200 mg bid for 10 days (very expensive)
b) IV immunoglobulin against C. difficile 400 mg/kg q3 wk (currently
under investigation)
c) probiotic 2 hours after antibiotics
6. Refer to a gastroenterologist for further treatment and consideration of
fecal transplant

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Hepatitis illnesses
Hepatitis A (HAV) illness

I. Description

A. Transmission route is fecal-oral from contaminated foods or people

with disease that handle food
B. Incubation period is 2 to 6 weeks
C. The disease is self-limiting and usually resolves within 4 to 8 weeks
D. Confers immunity with no lasting sequelae or damage to the liver
E. People at risk
1. Household contacts
2. Travelers to underdeveloped countries
3. IV drug users
II. Signs and symptoms

A. Anorexia, N/V
B. Low-grade fever with myalgia and flulike symptoms
C. Aversion to cigarette smoke
D. Dark, tea-colored urine that foams with gentle shaking
E. Clay-colored stools
F. Icteric sclera, jaundice, itching
G. Abdominal pain, liver tenderness and enlargement
III. Diagnostic tests

A. Hepatitis panel
B. Anti-HAV IgM and IgG
C. AST/ALT
D. Interpretation of tests
1. IgM anti-HAV: acute marker of infection, peaks in the first week
(before symptoms) and declines within 6 months of infection

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 2. IgG anti-HAV: marker of remote infection, not acutely infectious;
peaks after 1 month; may persist for years and indicates immunity
after infection; not a reliable marker after immunization
IV. Nonpharmacologic treatment

A. Supportive care with treatment for any symptoms

B. Bed rest
C. No work during acute phase with fever, fatigue, or jaundice; this
could last 2 months or more
V. Pharmacologic treatment

A. Avoid drugs metabolized in the liver

B. Hydroxyzine 10 to 25 mg tid prn or prochlorperazine 5 to 10 mg tid
prn for N/V
C. HBIG can be given within the first 2 weeks of diagnosis to infected
person and close contacts to decrease symptoms
D. Encourage vaccination for hepatitis B

Hepatitis B (HBV) illness

I. Description

A. Transmission is through blood, blood products, sexual contact, IV

needles, perinatal contact, semen, and wound exudate
B. Incubation period is 6 weeks to 6 months
C. Has acute and chronic states that are incurable, although remission
can be attained with pharmacologic therapy; after antibodies are
developed, the person has an increased risk of reactivation of illness; if
antibodies are cleared, the chance of reactivation is minimal
D. May lead to liver damage and cirrhosis
II. Signs and symptoms

A. Onset can be sudden or gradual and mimic flulike symptoms

B. Fleeting rash and hives with pruritis (less common)
C. Myalgia, malaise; easily fatigued
D. N/V/D and occasionally fever

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 E. Abdominal pain in the RUQ or epigastrium, increased with jarring
F. Liver tenderness and enlargement; jaundice
III. Diagnostic testing

A. Hepatitis panel (if hepatitis status is unknown, the person may have
concomitant HCV or HAV infection superimposed on HBV infection)
B. HBsAG, HBeAG
C. IgM anti-HBc
D. HBV DNA with reflux
E. Liver function tests (see Chapter 4, Liver)
F. PT/PTT, CBC
IV. Interpretation of hepatitis testing

A. HBsAg: first indication of infection and required for diagnosis

1. Appears in serum 2 to 10 weeks after exposure; persists throughout
the first 6 months
2. Presence of antigen indicates an infectious state
3. Persistent circulating HBsAg for >6 months indicates chronic HBV
B. HBeAg: indicates acute infection and active viral replication; if
continues after 3 months, this shows increased risk for active liver
disease
C. IgM anti-HBc: indicates new/acute infection; required for diagnosis
and is present <6 months after disease diagnosed
D. HBV DNA: indicates viral load
E. If the above tests are positive, also obtain the following:
1. HBeAb (presence of antibodies): used to monitor the course of
infection and treatment
2. IgG anti-HBc: indicates chronic hepatitis or superimposed acute
hepatitis from another cause; does not indicate an infectious state
3. HBsAb or anti-HBs: test for antibodies (protection identity) after
vaccination series; anti-HBc indicates recovery and immunity from
natural disease
4. Tests for immunity/protection

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 a) anti-HBs ≥10 mIU/ml indicates protection after hepatitis immunization
series of three injections
b) if anti-HBs is <10 mIU/ml on two separate occasions after “on-time
immunization series” at 0, 1, and 6 months (this does not indicate age)
and a titer was performed 2 months after the second series was
completed: write a letter stating what was done and that the person is
not protected against hepatitis B and has a window of 10 days after
exposure to get HBIG in order to stay protected
V. Treatment

A. Goals of treatment: reduce inflammation, prevent complications,

prevent further transmission
B. Referral to a hepatologist or gastroenterologist who specializes in
hepatitis treatment; as PCP, you may have to manage incidental
illnesses and side effects of treatment
C. Symptomatic treatment for N/V and malaise (avoid drugs
metabolized by the liver)
1. Can use B6 and ginger or peppermint for nausea
2. Soft, bland diet and oral rehydration solution (see Table 10-3) to
prevent dehydration
D. No acetaminophen or NSAIDs unless approved by a specialist
E. Bed rest
F. Monitor liver function tests, especially AST/ALT, and collaborate with
a specialist
G. Screen for HCV if the patient was born between 1945 and 1965 or is a
war veteran from the Vietnam era
H. Immunize for HAV
I. Postexposure prophylaxis for close contacts
1. Unvaccinated person: HBIG (0.06 ml/kg) and initiate hepatitis B
vaccine series (do not give immunizations at the same sites)
2. Completed series and is responder: no treatment
3. Known non-responder
a) HBIG 2 doses 1 month apart or

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 b) HBIG 1 dose and reinitiate vaccine series (do not give vaccine at the same
sites)

Hepatitis C (HCV)

I. Description

A. Transmission through blood products or injury with or sharing of

contaminated needles/syringes and contaminated medical supplies.
Possible transmission via high-risk sexual activity but may be related
to drug use and having multiple partners.
B. Incubation period is 14 to 140 days
C. The person may be asymptomatic when first exposed and symptoms
may not develop for ≥20 years
D. 40% of infected people have no risk factors
E. No vaccine available
F. Chronic HCV is related to significant liver disease and hepatocellular
carcinoma
G. People at high risk for liver disease and cirrhosis
1. People aged >40 years
2. People coinfected with HBV/HIV
3. Alcohol use or abuse
4. African-American males
II. Signs and symptoms: most patients with HCV are asymptomatic; if symptomatic, symptoms
are usually nonspecific and include the following:

A. Fatigue, weakness, weight loss

B. Nausea, anorexia
C. Myalgias and arthralgias
III. Diagnostic tests

A. Liver function tests (see Chapter 4, Liver) and hepatitis panel if unsure
of type
B. Hepatitis C antibody is specific for HCV
C. HCV RNA qualitative and quantitative with reflex genotyping: will

375
 determine the viral load and the genotype of HCV (genotypes 1 and 4
require longer treatment periods and are associated with a higher
incidence of liver damage)
IV. Treatment

A. Referral to a hepatologist or gastroenterologist who specializes in

hepatitis treatment
B. Hepatitis A and B immunizations and keep all other immunizations
up to date

Liver disease

I. Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)

A. NAFLD: hepatic steatosis without evidence of inflammation

B. NASH: hepatic steatosis associated with hepatic inflammation; similar
to alcoholic steatohepatitis (more likely to develop cirrhosis)
II. Description: increased presence of fat in the liver caused by abnormal lipid retention within
hepatic cells; will eventually cause liver enlargement and failure

A. Occurs in patients who do not abuse alcohol

B. Partially reversible condition
III. Diagnostic criteria

A. Alcohol consumption in amounts less than those considered

hepatotoxic
B. Absence of evidence of other hepatic diseases or disorders
C. Liver biopsy shows macrovesicular steatosis or steatohepatitis
D. Seen more often in women than in men
E. Seen more often in individuals with the following:
1. DM
2. Obesity (BMI > 30) with insulin resistance
3. Hyperlipidemia (primarily hypertriglyceridemia)
F. Most common cause of elevated liver enzymes
G. Has been found in children secondary to obesity and inactivity
IV. Signs and symptoms

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 A. Most patients are asymptomatic with vague complaints of fatigue or
malaise
B. Fullness in the RUQ and hepatomegaly (usually the only positive sign)
C. Acanthosis nigricans may be present in children
V. Diagnostic testing

A. Liver enzymes (see Chapter 4, Liver)

1. ALT/AST may be elevated but <2 times the normal
2. GGT may be mildly increased if alcohol abuse suspected
B. CBC, PT/PTT
C. Hepatitis panel
D. Liver biopsy (gold standard)
E. Liver U/S
VI. Treatment: referral to a hepatologist for management; if treated and the cause is removed,
prognosis is good and probability for progression to cirrhosis is decreased

A. Encourage weight loss

B. Encourage regular exercise
C. Antioxidants (e.g., vitamin E) and omega-3 fatty acids
D. Control DM and hyperlipidemia
E. Coffee has been found to be liver protective
F. Immunizations for HBV and HAV, keep other immunizations up to
date

Cirrhosis of the liver

I. Description: scarring of the liver with decreased function; hepatocellular fibrosis that
progresses to portal HTN and hepatic failure; considered the final phase of liver disease; usually
results from alcoholic liver disease, NAFLD, NASH, or chronic viral infection

A. Precancerous condition with an increased risk of hepatocellular cancer

B. Irreversible condition
II. Signs and symptoms

A. Many patients are asymptomatic; however, when symptoms occur,

they are usually progressive

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 B. Early symptoms
1. Fatigue and weakness
2. Poor appetite, nausea, abdominal pain, and weight loss
3. Telangiectasia
C. Later symptoms
1. Edema in legs and ascites in the abdomen; jaundice and itching
2. Venous hum over the umbilicus (indicates portal HTN)
3. Red color on the palms of hands, easy bruising, and abnormal bleeding
4. Pale-or gray-colored stools
5. Asterixis (flapping tremor)
6. In men: impotence, gynecomastia, and decreased testicle size
III. Diagnostic testing

A. Liver enzymes (see Chapter 4, Liver)

B. CBC, PT/PTT
C. Liver biopsy
IV. Treatment is referral to a hepatologist: maintain up-to-date status of all immunizations,
including HBV and HAV

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Bariatric surgery
I. Candidates for bariatric surgery

A. People with stable medical problems such as DM, dyslipidemia, HTN

B. People with BMI in range of >35 to 40
C. Well-motivated people willing to pursue life-long changes
II. Adverse effects related to bariatric surgery

A. Dumping syndrome: undigested contents of the stomach are

“dumped” into the small intestine too quickly (usually caused by too
much sugar or fatty foods), which causes nausea, weakness,
lightheadedness, and abdominal cramps
B. Protein calorie malnutrition (PCM) with severe decrease in
macronutrient absorption; seen with malabsorption-type surgeries
C. Osteoporosis due to rapid weight loss and decreased vitamin D and
calcium intake
D. Iron-deficiency anemia or B12 deficiency secondary to loss of stomach
surface area, causing decreased natural absorption
E. Kidney stones (oxylate type)
F. Gallstones secondary to rapid weight loss (increased cholesterol
secretion into bile and decreased emptying of the gallbladder)
G. Incisional hernias occur more frequently with an open procedure
H. Internal hernia caused by small bowel pocketing into the abdomen; a
more life-threatening event
I. Infection
III. Primary care management after surgery (especially if surgical team not available)

A. Continue to monitor current medical problems that were present

before surgery (e.g., DM, sleep apnea, hyperlipidemia,
NASH/NAFLD)
B. Monitor weight loss with office scale and home scale (try to weigh at
the same time qd and with the same clothing/shoes); very rapid weight
loss will lead to dehydration, weakness, and skin and nail changes

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C. Monitor medications (see below for medications to avoid)
D. Monthly chemistry profile to monitor albumin levels, creatinine, and
electrolytes until stable and then annually
E. CBC q1-3 mo to monitor anemia, which may not be evident for up to 6
months; then monitor annually to detect iron or B12/folate deficiency
F. Vitamin and mineral replacements
1. Oral iron preparations may not be tolerated because of GI symptoms
and may not be absorbed, necessitating parenteral preparations; if
using oral preparation, do not use extended-release preparations.
Suggested iron replacement is 27 mg in the evening with vitamin C 500
mg.
2. B12 500 to 1000 mcg IM monthly, if needed
3. Folate deficiency is less reported but should be considered;
supplement with folic acid 1 to 5 mg qd
4. Daily use of fat-soluble vitamins A, D, E, and K
a) vitamin A 10,000 IU/day
b) vitamin D 800 to 1200 IU/day
c) vitamin E 1000 IU/day
d) vitamin K 300 mcg/day
5. Calcium supplements 1200 to 1500 mg with meals for better absorption
6. Plastic surgery may be needed after surgery to remove redundant skin
flaps to decrease skin rashes and infections; consider about 6 months
after initial surgery
G. Medications and medication preparations that are acceptable after
bariatric surgery (this is a general list, please review the recommended
list from the surgical team)
1. Liquid forms of medication are preferred because of better absorption
over a smaller surface area
2. Immediate-release medications are safer and better absorbed in the
stomach
3. Extended-or sustained-release products will not be absorbed because
of the decreased size and surface area of the stomach and shortened

380
 small intestine
4. Multivitamins with iron, calcium citrate, folic acid
5. B12 supplementation (usually with IM injections)
6. Ursodiol (Actigall) may be given to help prevent gallstones
7. Calcitonin-salmon (Miacalcin) nasal spray and raloxifene (Evista) for
the prevention of osteoporosis
H. Medications to avoid after bariatric surgery (follow surgeon’s
recommendations)
1. ASA and NSAIDs/corticosteroids because of possibility of gastric
ulcers and bleeding
2. Multicombination OTC, because these products may not be absorbed
and may cause significant side effects
3. Bisphosphonates secondary to increased potential for gastric
ulcers/bleeding
4. Anticoagulant therapy will need to be monitored closely, because
weight changes can affect dosing schedules
5. Alcohol should be limited because of increased absorption
6. Gemfibrozil is associated with gallstones
I. Medications with decreased absorption
1. Enalapril, metoprolol, ramipril
2. Ketoconazole
3. Lamotrigine
4. Metformin
5. Niacin, simvastatin
6. Quetiapine (Seroquel)
7. Zolpidem (Ambien)

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C H A P T E R 11

382
Gynecologic conditions
Screenings and pap smears

Screening guidelines for women’s services

I. Because cervical cancer is very slow growing, it has been found that a long interval between
Pap tests is safe; however, the frequency of Pap tests is still at the provider’s discretion
II. Based on the patient’s risk factors, annual vulvovaginal and speculum examinations are still
indicated to detect other disease processes
III. Mammography has been reviewed, with new criteria for initial and routine scanning
developed on the basis of age, PMH, and FH
IV. See Table 11-1 for a comparison of Pap smear, BMD, and mammography screening
guidelines of the U.S. Preventive Services Task Force (USPSTF) and American Congress of
Obstetricians and Gynecologists (ACOG)

Table 11-1
Screening Guidelines: Pap Smear, Mammography, and BMD

USPSTF ACOG
Pap screen at age 21-65 yrs: q3yr Pap screen at age 19-20 yrs if indicated
or Pap screen at age 21-29 yrs: q3yrs
Pap screen and HPV test at age 30-65 yr: q5yr Pap screen and HPV test age 30-64 yrs: q5yr or Pap
screen q3yr

No Pap screen No Pap screen

• Age <21 yrs • Age > 65 yrs and past three screens were
• Age > 65 yrs with no increased risk (last two negative within 10 yrs
Paps negative within 5-10 yrs) • Hysterectomy for noncancerous reasons
• Hysterectomy for noncancerous reasons

No screen for cervical cancer with HPV test alone or in
combination with Pap if age <30 yrs
Annual clinical breast and pelvic examinations
Mammography q2yr between ages 50-74 yrs
BMD screen if age ≥65 yrs: q2yr
BMD screen if age ≥60 yrs: q2yr if high risk (history of fracture
and/or one or more risk factors*)
GC/chlamydia screen at age <25 yrs and if sexually
active
Annual clinical breast and pelvic examinations
Mammography q1-2yr starting at age 40 yrs and
annually after age 50 yrs
BMD screen at age ≥65 yrs: q2yr
BMD screen at age ≥60 yrs: q2yr if high risk (e.g., low
BMI*, Hx of previous fracture, age)

*
Low body weight is the best predictor for increased risk of fracture.

Interpretation of abnormal pap smears

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I. If Pap results are unsatisfactory for any reason: repeat test in 3 months
II. If Pap has negative cytology but HPV is positive, repeat in 3 months and if HPV is negative,
return to testing q2-3yr; if still positive, repeat again in 3 months, and if still positive, refer to
GYN
III. If Pap smear is ASC-US but negative for HPV, repeat in 1 year and if HPV is negative, return
to testing q3yr. If Pap is ASC-US and HPV is positive, repeat in 3 months and if HPV is negative,
return to testing q3yr; if HPV is still positive, repeat again in 3 months, and if still positive, refer
to GYN
IV. If Pap is LSIL and HPV is positive, repeat in 3 months; if HPV is negative, repeat again in 3
months and if still negative, then routine screening (see Table 11-1); if either repeat test is
positive for HPV, refer to GYN
V. If Pap is HSIL or AGC, refer to GYN regardless of the HPV status

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Contraception
Contraceptive methods

I. External methods: male and female condoms

A. Advantages
1. Inexpensive and reduce the risk of STIs
2. 85% effective in preventing pregnancy if used correctly; using
spermicide will increase effectiveness
B. Disadvantages
1. May cause skin irritation from latex allergy
2. May interrupt foreplay and may rupture during intercourse
3. Must be used correctly to prevent semen from escaping into the vagina
II. Barrier methods: diaphragms, cervical caps, sponges

A. Advantages
1. Easy to use and accessible; some benefit in reducing the risk of STIs
2. 85% to 95% effective in preventing pregnancy, especially if spermicide
is used
B. Disadvantages
1. Pelvic “heaviness” if left in too long
2. May cause vaginal discharge from irritation, spermicide, or latex
allergy; may increase vaginal infections
3. If not used correctly, can increase the possibility of pregnancy
III. Intrauterine devices (IUD): long-term method of contraception appropriate for women who
want reversible contraception, have difficulty remembering to take daily medicine, and are at a
low risk of infection (i.e., monogamous relationship or very few sexual partners)

A. Copper-T (nonhormonal)
1. Inserted for up to 10 years; can be removed and then reinserted
2. No change in menstrual cycles, decreases the rate of ectopic
pregnancy, and can be used as an emergency contraceptive (EC)
3. Does not provide protection from STIs, has increased possibility for

385
 infection (especially if multiple partners), must be inserted in office
setting
B. Levonorgestrel (Skyla)
1. Inserted for 3 years; can be removed and then reinserted
2. Can be used in nulliparous and parous women and at >6 weeks
postpartum
3. Does not protect against STIs, cannot be used for EC, increased risk for
infection if multiple partners, must be inserted in office setting
C. Levonorgestrel (Mirena)
1. Inserted for 5 years; can be removed and then reinserted
2. May cause decreased menstrual cycles and decreased menstrual flow
and increased acne or hair growth
3. Does not protect against STIs, increased risk for infection if multiple
partners, cannot be used for EC, must be inserted in office setting
D. Implants (Etonogestrel [Implanon or Nexplanon]) are long-term
contraception methods appropriate for women who want reversible
contraception and have difficulty remembering to take pills daily
1. Advantages
a) inserted for 3 years into the upper inner arm; can be removed and
replaced
b) may cause decreased menstrual cycles and decreased blood flow
2. Disadvantages
a) does not provide protection from STIs, must be inserted in office
setting
b) may have decreased efficacy in women with BMI > 30 kg/m2
c) may cause increased acne or hair growth
E. Contraindications
1. Breast cancer, liver disease, DVT/VTE
2. Irregular heavy vaginal bleeding
IV. Injectable medroxyprogesterone (Depo-Provera)

A. Advantages

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 1. Requires 1 injection q12wk
2. Decreases anemia and can be used with a history of DVT, PE, smoking,
CV disease, DM, migraine, seizures
3. Initial injection should be given
a) within the first 5 days of menstrual cycle or
b) within 5 days postpartum if not breastfeeding or
c) sixth postpartum week if breastfeeding
d) if >13 weeks since last injection, perform pregnancy test before giving
the next one
B. Disadvantages
1. Must go to the clinic for injection
2. Weight gain, H/A, depression
3. Irregular bleeding
4. Bone loss greatest in first 2 years of use and minimal after that;
recovery of BMD occurs rapidly after stopping medication
5. No protection against STIs
C. Contraindications
1. Obesity
2. Suspected pregnancy or abnormal bleeding
3. Depression
D. Additional points
1. Must take calcium supplement daily, especially if cycles stop
2. Consider BMD
V. Progestin-only pills (POPs)

A. Advantages
1. Norethindrone and norgestrel are common formulations; taken qd
with no “dummy pills”
2. Can be used during lactation and by women with contraindication to
estrogen (e.g., ≥35 years of age who smoke, or have migraines with
aura)

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 3. May decrease menstrual cycles and PMS
4. Fertility is reestablished quickly after stopping pill
5. Initiate on the first day of the menstrual cycle or within the first 5 days
of the cycle; using back-up protection is not indicated unless POPs are
started at other times during the menstrual cycle
B. Disadvantages
1. No protection against STIs
2. Must take at the same time qd; missing daily pills decreases
effectiveness and increases the risk of pregnancy
3. Unscheduled bleeding episodes may occur
C. Contraindications
1. Breast, uterine, or cervical cancer
2. Liver disease, stroke, VTE/DVT
3. Irregular or heavy menstrual cycles
VI. Combined oral contraceptives (COCs)

A. Ethinyl estradiol is the most common estrogen component and may

range from 10 to 35 mcg
B. Progestin may consist of various types: norethindrone, desogestrel,
levonorgestrel, drospirenone
C. Advantages
1. Relieves PMS symptoms, decreases menstrual cramping and bleeding,
and can improve acne
2. May provide some protection against ovarian cancers and PID
3. Can manipulate menstrual cycles by decreasing the number of cycles
per year depending on the pill pack (e.g., monthly, quarterly, or
longer)
4. Dosing schedule consists of daily pill to establish routine
D. Disadvantages
1. Must take at the same time qd; missing pills increases the chance for
pregnancy and a back-up method must be used
2. Missing >1 pill may cause breakthrough bleeding (BTB)

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 3. No protection against STIs; if high risk, should consider condoms
4. Effectiveness can be decreased with some medications (e.g.,
antibiotics)
5. Estrogen increases the risk of VTE, CVA, and MI; the new lower-dose
estrogen pills may decrease the risk of VTE and other systemic
symptoms related to hormonal therapy (e.g., bloating, breast
tenderness, nausea) but may increase BTB
E. Contraindications
1. VTE, DVT
2. Migraine with aura
3. Breast or cervical cancer
4. Smoking after 35 years of age
5. Liver or heart disease
VII. Ortho Evra Patch

A. Advantages
1. Weekly application; is easy to apply and has good adherence
2. If used correctly, 99% effectiveness
3. When prescribing, add extra patch in case one patch comes off
B. Disadvantages
1. Weight must be <180 lb
2. Patch may irritate the skin and/or may come off unexpectedly
3. No protection against STIs
C. Contraindications: same as COCs
VIII. NuvaRing

A. Advantages
1. Patient inserts vaginal ring 3 wks/mo; very flexible and easy to insert
2. If used correctly, 99% effective against pregnancy
B. Disadvantages
1. May accidently be expelled and some patients can feel “object in
vagina” during intercourse

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 2. No protection against STIs
C. Contraindications: same as COCs

P r a c t i c e Pe a r l s f o r C o n t r a c e p t i o n

• Before prescribing hormonal contraceptives, perform H&P, which may include Pap smear,
pregnancy test, and STI testing.
• Lower-dose COCs with third-and fourth-generation progestins (e.g., desogestrel and
drospirenone) have decreased androgenic activity and fewer side effects than first-and
second-generation progestins (e.g., norethindrone and levonorgestrel).

• Benefits include decreased acne, minimal weight gain, decreased hair

growth, decreased LDL levels, and increased HDL levels.
• Adverse effects include increased risk for VTE.
• Do not use COCs if there is any history of venous thrombosis, cardiovascular disease, or
migraine with aura.

• Taking an ASA daily with COCs may decrease the risk for all users, but
this has not been proven.
• Caution younger women taking COCs against smoking.
• If BTB occurs:

• Patient <35 years who smokes: try using pills with increased progestin
activity
• Patient >35 years who smokes: use progestin-only contraceptives such
as levonorgestrel IUD (Mirena, Skyla), implants, medroxyprogesterone
(Depo-Provera) IM, or POPs; caution woman to stop smoking

Tips on taking oral contraceptives

I. Following are a few helpful comments on pill use (also see Table 11-2)

A. Start the pack on the first day of the menstrual cycle or the first
Sunday after menses start; use a back-up contraceptive method for the
first pack of pills
B. Take the OCs at the same time qd; if N/V occurs, take with food or at

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 hs
C. The greatest risk of pregnancy usually occurs just before or just after
the hormone-free interval
D. Combined OCs need to be taken for at least 7 consecutive days to
prevent ovulation; always consider emergency contraception (EC) due
to missed pills
E. If 1 pill is missed during the cycle and no other pills have been missed
the prior month, then take the pill as soon as remembered and there is
no need for a back-up method of birth control for the remainder of the
pill pack.
F. If ≥ 2 pills are missed in a row, take one as soon as remembered and
throw out the other pills that were missed and continue the pill pack.
Use back-up birth control for the next 7 days. If >2 pills are missed in
the last 2 weeks of the pill pack, take 1 pill daily until the active pills
are finished and then immediately start a new pill pack. No back-up is
needed after new pill pack is started.
G. If ≥3 pills are missed, menses will probably start; continue taking 1 pill
qd until the active pills are finished and then start a new pack; use a
back-up method for 7 days of the new pack
H. Consider EC if ≥2 pills are missed in the first 2 weeks of the cycle and
the woman had unprotected sex in the 5 days before missing the pill
I. If 1 or more POP is missed, take it immediately even if it means taking
2 on the same day. Use back-up method of contraception until pills
have been taken consistently for at least 2 days. Always consider EC
with unprotected sex.
J. If >15 weeks from last Depo-Provera injection, check for pregnancy and
if negative give injection and use back-up method of contraception for
the next 7 days.
II. Notify the clinician immediately if any of these signs occur after starting OCs

A. Severe chest pain

B. Severe H/A or paresthesia
C. Change in vision
D. Pain or swelling in legs or SOB and tachycardia

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 E. Severe abdominal pain
III. Missing one period while taking OCs is no reason for concern; if two periods are missed,
perform a pregnancy test
IV. Always use condoms; OCs do not protect against STIs caused by skin-to-skin contact
V. Use a back-up method of birth control when taking antibiotics (this may not cause decreased
efficacy of pill, but if any pills are accidently missed during illness, then the antibiotic will be
blamed for the pregnancy).
VI. Emergency contraception (always perform pregnancy test before initiation)

A. Plan B and Yuzpe regimen prevent pregnancy by inhibiting ovulation,

not by disrupting the pregnancy; Ulipristal and copper IUD could
affect an established pregnancy (this is controversial)
B. Types of available emergency contraceptive pills (ECP) (Table 11-3)
1. Levonorgestrel (Plan B one-step OTC): take 1 pill within 72 hours (can
be used up to 120 hours but efficacy decreases)
a) if vomiting occurs, repeat dose
b) may be less effective with obese women (BMI > 30 kg/m2)
2. Ulipristal (Ella [prescription only]): 1 tab within 120 hours
a) repeat dose if vomiting occurs
b) may be less effective with obese women (BMI > 30 kg/m2)
3. Copper IUD must be inserted within 5 days (off label in US)
a) no decreased effectiveness with obese women
b) can be left in for up to 10 years
4. Yuzpe regimen (see Table 11-3) uses common OCPs in a particular
amount (no prepackaged pills are available for the regimen)
a) the dose is based on progestin content; ∼100 mcg ethinyl estradiol
and 0.5 mg of levonorgestrel; depending on the type of pill, 2 doses are
taken 12 hours apart
b) consider pretreatment with an antiemetic 1 hour before each dose
c) less effective and has more side effects but is usually more accessible
and provides more privacy to women
d) may be less effective with obese women (BMI >30 kg/m2)
C. If vomiting occurs within 3 hours of taking ECP, give an antiemetic

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 and repeat the dose
D. Use barrier method for 14 days or until the next period, then resume
regular form of birth control
E. Regular menses may occur up to 1 week earlier after taking hormonal
ECP
F. Relative contraindications: active migraines with aura, other
neurologic conditions, and history of VTE
G. If no menses for 3 weeks, perform a pregnancy test; if no menses for 2
months, follow-up with PCP
Table 11-2
Common OC Selections

Side Effects Alternatives

Acne, hair growth OCs with higher estrogen activity to androgenic activity or decreased androgenic
activity: Loestrin, Ortho-Cyclen, Demulen-35, Ortho Tri-Cyclen, Yasmin

Weight gain OCs with lower estrogenic and androgenic activity: Ortho-Novum 1/35, Ovcon-35,
Yasmin, YAZ

Fluid retention OCs with lower estrogenic activity or estrogen doses: Loestrin 1/20 or 1.5/30

H/A, nausea OCs with lower estrogenic effects or estrogen doses: Alesse, Mircette, Loestrin; also take
pills at night to decrease nausea

Breakthrough bleeding:
-During the first 14 days of the
cycle
-During the last 14 days of the
cycle (before taking inert pills)
-Anytime during the cycle
OCs with higher endometrial activity: Mircette, Loestrin, Ovcon-35, Ortho-Cyclen,
Ortho Tri-Cyclen
OCs with higher progestin and/or androgenic activity: Lo-ovral, Levlen, Ortho-Novum-
35, Estrostep, Ortho-Cyclen
Estrostep, Loestrin, Cyclessa, Ortho-Novum 1/35

Skin rash or pruritus Usually occurs from inactive ingredients; switch to pills with different inactive
ingredients

Decreased libido OCs with increased androgenic activity: Alesse, Levlen, Loestrin 1.5/30

Amenorrhea Determine cause and correct; may need to change the type of estrogen or progestin

Breast tenderness OCs with lower estrogen dose or higher androgenic activity: Loestrin 1.5/30 or 1/20,
Levlen, Levora 0.15/30

Dysmenorrhea OCs with higher progestational activity: Loestrin 1 mg/10 mcg, Loestrin 1.5/30 or 1/20,
Demulen 1/35

Smokers aged ≥35 yrs NO COC†; can use Micronor, IUD, or implants

Suggested contraception for specific medical conditions

Controlled DM without OCs with lower estrogenic and androgenic activity: Demulen-35, Alesse, Micronor; or
vascular complication with use copper IUD

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 vascular complications Copper IUD, oral progestins, implants, avoid estrogen containing products and Depo-
Provera

HTN (controlled) IUDs, or Micronor; no COC†

Depression OCs with lower progestin activity: Ortho-Tri-Cyclen, Yasmin, Ovcon-35; avoid long-
acting progestins—may exacerbate depression

Migraine with aura Copper IUD or Micronor, no COC †

Migraine without aura ≤35 years: copper IUD or POPs; if no worsening of H/A can try OCs with lower
estrogenic activity or lower estrogen doses: Loestrin 1 mg/10 mcg, Loestrin 1/20,
Micronor, Mircette, Seasonale/Seasonique
≥35 years: copper IUD or POPs, avoid estrogen-containing products

Menstrual migraine If H/A during the last 7 days of pack, consider adding low-dose estrogen on 5/7 of those
days; avoid triphasic OCs

Seizure disorder Depo-Provera and IUDs; avoid oral estrogen and progestins, consider barrier method

Dyslipidemia OCs with levonorgestrel or, ↓dose norethindrone: Ortho-Cyclen, Ovcon-35, Desogen;
avoid long-acting progestins

Bariatric surgery IUDs, patch (if patient’s wt <90 kg), implants or vaginal ring; avoid oral contraceptives
unless banding or sleeve procedure was performed, then any type contraceptive can be
used

Postpartum Non-breastfeeding: avoid estrogen containing products for 42 days, then no restrictions
Breastfeeding: IUDs, POPs

†Combined
oral contraceptive (i.e., containing both estrogen and progestin).
*OCs
are listed by brand names.

Table 11-3
Contraceptives for Emergency Contraception

Dosing (Should Begin Within 120 h of

Formulation Brand Name
Unprotected Intercourse)
Levonorgestrel 0.15 mg + ethinyl Nordette 4 light-orange pills; repeat in 12 h
estradiol 30 mcg

Levonorgestrel 0.1 mg + ethinyl Alesse, Aviane 5 orange pills; repeat in 12 h

estradiol 20 mcg

Levonorgestrel + ethinyl estradiol Trivora 4 pink pills; repeat in 12 h

triphasic dosing

Levornorgestrel 0.15 mg + ethinyl Seasonique, 4 light blue-green pills; repeat in 12 h

estradiol 30 mcg Seasonale

Levonorgestrel 0.1 mg + ethinyl LoSeasonique 5 orange pills; repeat in 12 h

estradiol 20 mcg

Levonorgestrel 0.09 mg + ethinyl Lybrel 6 yellow pills; repeat in 12 h

estradiol 20 mcg

Levonorgestrel 1.5 mg Plan B (OTC) 1 pill within 72 h

Ulipristal 30 mg Ella 1 pill

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Copper IUD Inserted within 120 h

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Conditions related to menstruation
Premenstrual syndrome (PMS)/premenstrual dysphoric disorder
(pmdd)

I. PMS

A. Cluster of symptoms that are both physical and emotional, occurring

in the latter half of the menstrual cycle (e.g., last 10 days); do not limit
daily activity
B. Characterized by the following:
1. Depression, irritability, increased appetite
2. Acne, greasy or dry hair
3. Bloating and weight gain (>2 to 5 lbs), breast tenderness
4. H/A, fatigue
C. Resolves shortly after period begins
D. Treatment is usually supportive, with education, lifestyle changes,
and nutritional changes (see PMDD below)
II. Premenstrual dysphoric disorder (PMDD)

A. Characterized by more emotional than physical symptoms that limit

daily activity
B. PMDD criteria: for most menstrual cycles for the last year, ≥5 of the
following symptoms occurred during the last phase of the menstrual
cycle and resolved a few days into the menstrual cycle
1. Markedly depressed mood with feelings of hopelessness
2. Marked anxiety, tension, feelings of being “excitable” and “on edge”
3. Labile mood with mood swings, sadness, and increased sensitivity
4. Marked irritability, anger, and sense of being “out of control”
5. Decreased interest in usual activity (e.g., work, school, home),
lethargy, and lack of energy
6. Difficulty concentrating, insomnia
7. Increased appetite and food cravings with weight gain

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 8. May have other physical symptoms (e.g., breast tenderness, swelling
in hands, and headaches)
III. Treatment for PMS/PMDD

A. General
1. Lifestyle changes and identifying patterns of recurring symptoms
2. Cognitive and behavioral therapies
3. Physical exercise starting when symptoms begin
4. Decreased caffeine, alcohol, and sodium intake at least 2 weeks before
menses
5. Warm moist heat to the abdomen
B. Consider nutritional/herbal supplements qd beginning about 5 days
before the start of the menstrual cycle; these may be taken qd rather
than just before menses
1. Evening primrose oil may help decrease bloating, depression,
irritability
2. Daily calcium 1200 mg, vitamin B6 50 to 100 mg, and magnesium 400
to 1000 mg may help with fatigue, edema, H/A
3. Vitamin E 400 to 800 IU may decrease depression, breast pain, and
fatigue
4. Regular, frequent, small meals with increased complex carbohydrates
C. Drug therapy
1. Diuretics used only for patients who can document actual weight gain
before the menstrual cycle; any diuretic will work at the lowest dosage;
start before weight increases and stop after menses start
2. NSAID of choice: start 2 to 3 days before pain is expected and stop
about 2 to 3 days after menses start
3. SSRIs can be used in severe cases to improve mood swings, irritability,
anxiety, and depression
a) daily or cyclic dosing: (i.e., start 10 to 12 days before the next cycle and
stop 1 to 2 days after the menstrual cycle starts)
b) if symptoms not controlled, can increase the dose of daily SSRI
starting on day 10 before the next period starts

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 c) most commonly used: fluoxetine 10 to 20 mg, sertraline 50 mg,
citalopram 10 to 30 mg
4. Anxiolytics
a) started before symptoms and tapered off after menses start
b) commonly used: alprazolam 0.25 to 2.0 mg qd (start 1 to 2 days before
menses) or buspirone 15 to 60 mg qd (can start 10 days before menses)
5. OCs may stabilize hormonal fluctuations and relieve or eliminate some
symptoms
a) use low-dose COCs, monophasic pills (Yasmin should help control
weight gain)
b) can also use progesterone-only contraceptives to stabilize symptoms
(e.g., Depo-Provera or POPs)

Dysmenorrhea

I. Primary

A. Painful menstruation associated with ovulatory cycles

B. Usually associated with spasmodic pelvic pain, back pain, or leg pain
1. Starts on the first day of the menstrual cycle and decreases as the
uterine lining is shed
2. May improve as the girl ages; may stop or significantly decrease after
childbirth
C. Treatment
1. NSAIDs: start 1 to 2 days before menses starts and continue 1 to 2 days
into the cycle
2. COCs or progestin birth control methods
II. Secondary

A. Painful menstruation associated with reproductive disorder (e.g.,

endometriosis, adhesions, fibroids, adenomyosis); usually begins later
in life
B. May start several days before the menstrual cycle starts and may not
resolve until the cycle is finished; may worsen over time
C. Diagnosis is usually based on physical examination, pelvic U/S

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 D. Treatment is referral to GYN if symptoms not controlled

Menstrual migraines

I. Definition

A. For ≥3 cycles, cyclical migraine associated with menses, starting ∼2

days before menses and lasting ∼2 to 3 days into the cycle
B. Associated with the decrease in estrogen levels before menses
II. Signs and symptoms

A. H/A without aura

B. Other symptoms similar to chronic migraine (see Chapter 13,
Headaches, V,B)
III. Diagnostics

A. Similar work-up to chronic migraines (see Chapter 13, Headaches,

V,B)
B. H/A diary showing H/A before menses for ≥3 consecutive months
IV. Treatment

A. Abortive migraine treatment (see Chapter 13, Headaches, V,B) as

needed; if H/A is noted to be cyclic or if resolution is unsatisfactory,
then start prophylactic treatment
B. Prophylaxis
1. NSAIDs of choice: start 2 days before menses and continue 2 days (or
more) into the cycle
2. Triptans: started 2 days before the menstrual cycle and continued for 3
days (e.g., total of 5 days)
a) sumatriptan 25 mg tid
b) naratriptan 1 mg bid
c) zolmitriptan 2.5 mg bid
d) frovatriptan 2.5 mg qd/bid
3. Estrogen products (caution with older women; may need intermittent
dosing before the menstrual cycle)
a) transdermal estrogen patch 100 mcg, applied 1 to 2 days before the

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 menstrual cycle and left on for 5 days
b) COCs with a 28-day cycle of estrogen (e.g., Mircette), 91-day cycle of
low estrogen (e.g., Seasonique, Seasonale), or 21-day cycle of lower-
dose estrogen (e.g., LoEstrin)
4. Other medication/herbal therapy
a) fluoxetine 10 to 20 mg qd: start 2 weeks before menses and stop when
menses start
b) magnesium citrate 400 mg: take the first 5 days of menstrual cycle

Abnormal bleeding patterns

I. Abnormal uterine bleeding (AUB)

A. Definition: bleeding between menses, excessive bleeding, or any

postmenopausal bleeding
B. Causes
1. Ovulatory
a) occurs at regular intervals, usually associated with PMS symptoms
(breast tenderness, weight gain, mood swings); usually signals that
ovulation has occurred
b) there is an adequate amount of progesterone for endometrial
proliferation but inadequate estrogen for continued proliferation
c) endometrium becomes friable and heavy bleeding occurs
d) estrogen replacement should correct problem
e) common causes
(1) anatomic problems: tumors, infections, lacerations, pregnancy, or
complications from pregnancy
(2) bleeding disorders: idiopathic thrombocytopenic purpura (ITP), DIC,
leukemia, von Willebrand’s disease
(3) medications such as warfarin, aspirin, NSAIDs
(4) renal or liver disease
2. Anovulatory
a) occurs at irregular intervals with frequent spotting and infrequent

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 heavy bleeding; is not associated with PMS and usually occurs at the
extremes of reproductive life span
b) common causes
(1) puberty: immature HPO axis; usually takes about 20 months to
establish a normal pattern of menses
(2) childbearing years (16 to 40 years): pregnancy and complications of
contraceptives, adenomyosis, endometriosis, fibroids, endometrial
hyperplasia, polyps, PCOS, PID
(3) perimenopausal women tend to be hyperestrogenic with lower
progestin levels, which increases the risk for endometrial hyperplasia
and AUB
(4) smoking
C. Diagnostic testing
1. UCG/HCG
2. CBC, CMP, TSH, prolactin, liver function/hepatitis panel
3. Pap smear, STI testing
4. Pelvic U/S to determine endometrial lining and any abnormal masses
(if endometrial lining is >5 mm, endometrial biopsy is warranted)
D. Treatment
1. Progestin therapy: medroxyprogesterone 10 mg qd for 10 to 12 days
q4wks; start on day 16 or 21 of the cycle (e.g., first day of the menstrual
cycle is day 1)
2. Low-dose COCs
a) ≤18 years of age: 20 to 30 mcg ethinyl estradiol (EE)
b) 19 to 40 years of age: 10 to 35 mcg EE
c) ≥40 years of age: 10 to 20 mcg EE
3. With no systemic or organic cause for bleeding, assume bleeding is
anovulatory, but if bleeding is not controlled with hormones, look for
other causes of abnormal bleeding
4. Prolonged bleeding is suggestive of denuded uterine lining and can
lead to significant anemia

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 a) refer for hospitalization if Hgb <7 g/dl with orthostatic signs, patient is
in shock, or if pad count is >1 pad/h
b) Hgb 7 to 10 g/dl
(1) may give Premarin 1.25 mg qid until bleeding subsides (should be
within 72 hours), then start COCs qd for next 3 months or Lo/Ovral 1
tab qid for 4 days, tid for 3 days, bid for 2 weeks, then start a new pill
pack immediately
(2) may need to give antiemetics when using high-dose estrogen
products
(3) refer to GYN if bleeding continues or restarts after treatment
c) Hgb >10 g/dl
(1) monophasic OCs: 2 tab bid until bleeding slows, 1 tab bid until
bleeding stops, then finish pill pack; immediately start new pill pack
and take 1 tab qd for 2 to 3 cycles without stopping or having
withdrawal bleeding or
(2) if COCs are contraindicated, start POPs or medroxyprogesterone
(Provera) 10 mg qd for 10 to 12 days q4wks
(3) once bleeding has been controlled, start OCs or HRT for 6 months
5. Reevaluate anemia 1 month after starting iron replacement; increase
iron-rich foods (see Appendix A)
6. NSAIDs of choice will help reduce cramping, bleeding, or both;
caution patients to take with food
7. Abnormal bleeding may be a side effect of missing OCs; encourage
regular timing of pills
8. If scanty bleeding is noted during the pill-free interval and abnormal
bleeding occurs during the regular cycle, this may indicate progestin
excess; try increasing estrogenic activity or decreasing progestin
activity of COCs

Polycystic ovarian syndrome (PCOS)

I. Description

A. Hormonal disorder of the ovary and adrenal glands that occurs over
time (if rapid onset, consider cancer)

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 B. Associated with insulin resistance that causes excess testosterone and
virilization characteristics
C. Adolescents may present with irregular or absent menses; women
may present with difficulty getting pregnant or unexplained weight
gain
D. Long-term outcomes of untreated PCOS may include DM, HTN, heart
disease, and endometrial cancer
II. Signs and symptoms

A. Oligomenorrhea, irregular (e.g., either scant or heavy) menses,

secondary amenorrhea
B. Infertility or decreased fertility
C. Central obesity (few are underweight)
D. Signs of androgen excess
1. Hirsutism, mainly on the chest, abdomen, face, and nipples
2. Oily skin and increased acne
3. Alopecia (e.g., male pattern baldness)
E. Acanthosis nigricans
F. Insulin resistance with elevated levels of insulin followed by increased
glucose
G. Increased triglycerides with low HDL and HTN
III. Diagnostic testing

A. TSH
B. Prolactin (elevated levels indicate pituitary tumor)
C. LH/FSH ratio usually 2:1 (normal ratio does not exclude PCOS
diagnosis)
1. Elevated FSH level indicates premature ovarian failure
2. Elevated LH/FSH ratio indicates anovulation and PCOS
D. Elevated level of 17-hydroxyprogesterone (>1000 ng/ml) should be
evaluated further as it may indicate congenital adrenal hyperplasia
E. Total testosterone and DHEA are normally elevated; if testosterone
>200 ng/dl or DHEA >800 mcg/dl, this is more indicative of virilizing

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 adrenal tumor
F. Complete chemistry panel, 2-hour GTT (2-hour GTT >200 mg/dl
indicates insulin resistance), lipid panel
G. Pap smear and pelvic examination to identify any structural
abnormalities
H. Consider endometrial biopsy and pelvic transvaginal U/S (prolonged
estrogen stimulation can increase the risk of endometrial cancer)
I. UCG
IV. Treatment goals: reduce insulin levels, decrease testosterone production, and reestablish
normal hormonal balance

A. Weight loss (even 5% to 10% loss can help enough to restart menses)
B. Exercise
C. Metformin for insulin resistance; may also correct anovulation; usual
dose is 500 to 1000 mg bid
D. COCs to reestablish normal hormonal levels
1. Progesterone alone can be used (protects the endometrium from
unopposed estrogen)
2. Yasmin is the OC of choice because of the drospirenone component
which acts like spironolactone and blocks androgens
E. Hair removal techniques (e.g., electrolysis or waxing) or eflornithine
(Vaniqua) for removal of facial hair
F. Antiandrogens (e.g., spironolactone, finasteride) may decrease hair
growth and improve acne; effects may take 3 to 6 months to be noticed
G. Monitor FBG and GTT annually, lipid profile q1-3yr as indicated, and
BP on each visit
H. Refer to OB/GYN or infertility specialist if pregnancy is desired

Amenorrhea

I. Primary amenorrhea

A. Absence of menarche by 16 years of age with normal sexual

development or 14 years of age without sexual development
B. Causes

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 1. Athlete’s amenorrhea
2. Anorexia, bulimia
3. Pituitary lesions
4. Hereditary conditions
C. Signs and symptoms
1. Obvious abnormal growth and development of secondary sexual
characteristics (may look female but have male characteristics)
2. May have obstruction to menstrual flow with cyclic abdominal pain
3. History of excess exercise >2 hours qd
4. Extreme dietary limitations in protein, fat intake, or both
5. Weight <95 lbs
6. Increased hair growth and acne
D. Diagnostic testing
1. Examination to include height, weight, VS, and Tanner’s stage (see Box
2-1)
2. Breast and pelvic examination to assess for normal development
3. UCG/HCG, TSH, LH, FSH, DHEA, free and total testosterone
4. Question regarding drug use (illegal, prescription, and OTC)
5. Consider pelvic U/S or pelvic CT if unsure of internal structures
E. Treatment
1. If genetic or physical problem suspected, refer to a geneticist or
pediatric specialist
2. If amenorrhea is caused by too little body fat because of poor nutrition
or eating disorder, refer to both a nutritionist and pediatric psychiatrist
II. Secondary amenorrhea

A. Absence of menses for >3 months in a woman who previously had

normal cycles or absence for >12 months in a woman whose cycles
have been irregular
B. Causes
1. Central organ failure

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a) athlete’s amenorrhea
b) stress
c) severe eating disorders
d) posthormone suppression
e) pituitary lesions
2. Ovarian failure (e.g., premature or natural menopause or autoimmune
disorders)
3. End organ failure
a) cervical stenosis
b) uterine surgeries (e.g., ablation, D&C)
c) Asherman’s syndrome (e.g., intrauterine adhesions [scar tissue])
4. Anovulation (e.g., PCOS)
5. Pregnancy-related
a) intrauterine or extrauterine pregnancy
b) hydatidiform mole
c) missed abortion
6. Drug-induced
a) illegal drugs (e.g., “crack,” “meth,” cocaine, or heroin)
b) prescription drugs (e.g., haloperidol)
c) herbal products (e.g., any product that stimulates estrogen receptor
sites: red clover, black cohosh, DHEA, milk thistle, and ginseng)
C. Signs and symptoms
1. Central organ failure
a) galactorrhea
b) H/A, visual changes
c) decreased libido
d) weight loss, low body mass
2. Ovarian failure
a) hot flashes; vaginal dryness; dry, pale vaginal mucosa

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b) labile moods
c) weight gain
3. End organ failure
a) cyclic PMS without menses
b) abdominal bloating
c) pinpoint cervical os
4. Anovulation
a) hirsutism, acne
b) deepening voice
5. Pregnancy-related: enlarged abdomen with gravid uterus
D. Diagnostic testing
1. Pregnancy test (HCG, UCG)
2. Prolactin level (if having galactorrhea)
3. TSH, FSH, LH
a) if LH >10 mIU/ml and LH/FSH ratio >2:1, suspect PCOS
b) FSH >40 mIU/ml indicates menopause
4. DHEA and testosterone levels (if androgen excess is suspected); if
DHEA >700 ug/dL or testosterone >150 ng/dL, consider ovarian or
adrenal tumor
5. Pelvic U/S, especially if h/o uterine surgeries or if fails progestin or
COC challenge (i.e., no bleeding occurred with medications)
6. CT scan of the abdomen and pelvis, if indicated
7. Consider endometrial biopsy
8. Consider MRI pituitary if galactorrhea and H/A present
E. Treatment
1. See Figure 11-1 for evaluation of secondary amenorrhea
2. Prevent osteoporosis by encouraging calcium and vitamin D along
with weight-bearing exercise
3. Discuss hormone replacement and/or contraception if indicated

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4. If amenorrhea is due to overexercise (e.g., athlete’s amenorrhea)
a) decrease the amount of exercise time or change the training program
to allow more rest
b) increase daily calories up to 1500 to 2000 cal/day, calcium 600 mg with
each meal, and vitamin D 400 to 800 IU/day
c) start OCs to prevent bone loss and reestablish hormonal balance
d) if menses have not started after 3 to 6 months, refer to a gynecologist
5. If menstrual cycles do not start and vasomotor symptoms present
without HRT (and diagnosis is menopause), consider SNRI
6. If present, treat PCOS (earlier in this chapter) and/or thyroid disorder
7. Refer to an appropriate specialist

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 FIGURE 11-1 Evaluation of Secondary Amenorrhea.

Menopause

I. Description

A. Usually occurs between 45 and 55 years of age

B. Menopause can be related to the onset of atherosclerosis, osteoporosis,
DM, and weight gain

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 C. Perimenopause: the time between cycle irregularity and last menstrual
cycle; symptoms occur approximately 5 to 7 years before the cycles
cease
II. Signs and symptoms

A. Perimenopause: fluctuations in hormones lead to irritability, “hot

flashes,” irregular cycles, and vaginal dryness; may be inconsistent for
several years, with a cycle of normal menses followed by long intervals
of amenorrhea
B. Menopause
1. No menstrual cycles for 12 consecutive months
2. Vasomotor symptoms such as hot flashes/flushes, night sweats are
usually noticed first and may be succeeded by the following:
a) vaginal atrophy/dryness and irritation, recurrent vaginitis, decreased
labial size
b) frequent UTIs, stress incontinence, dysuria, frequency
c) dyspareunia, feeling of pressure in the perineum, ↓ libido
d) H/As, forgetfulness, or decreased concentration
e) mood swings, anxiety without reason, apathy
f) altered sleep patterns, loss of energy
g) weight gain in hips and thighs
h) ↓ skin elasticity with dryness and wrinkling
i) ↓ breast size and thinning of axillary, pubic, and leg hair
3. Vasomotor symptoms usually start to resolve about 2 to 3 years after
onset
III. Diagnostic testing may not be indicated if symptoms are consistent with menopause

A. FSH >40 mIU/ml (can fluctuate during perimenopausal period)

B. Estradiol <30 pg/ml (↓ estradiol and ↑FSH are indicative of
menopause)
C. LH 14 to 52 mIU/ml is indicative of menopause
D. TSH (to exclude thyroid dysfunction)
E. Prolactin level (if any galactorrhea)

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IV. Treatment

A. Perimenopause therapies
1. Emphasis should be on a healthy lifestyle
a) weight loss
b) exercise (aerobic, strength training, and weight bearing)
c) smoking cessation
d) decreased caffeine intake
e) increase intake of soy products and flaxseed
f) multivitamin qd
2. If cycles are sporadic and/or heavy and the woman is not a smoker and
has a low-risk profile, use low-dose (10 to 20 mcg estradiol) COCs for
cycle control
a) at age 50 to 52 years, check FSH on day 5 of pill-free week
b) if FSH is elevated in 2 consecutive months, can switch to low-dose
combined HRT (if patient wants to continue hormonal therapy)
3. Herbal therapies (see vasomotor symptoms below) can stimulate
estrogen receptors indirectly, thus causing unwanted side effects
related to estrogen (e.g., breast tenderness, bloating) and increasing the
risk of endometrial cancer. Just because it is herbal does not mean it is
safe.
4. Encourage patients to dress comfortably in layered clothing and avoid
extreme temperature changes
B. Menopause therapies
1. Short-term combined HRT may improve overall quality of life and
slow vasomotor symptoms (Table 11-4)
a) never give unopposed estrogen to any woman who still has a uterus; always
balance with progestin
b) HRT is not indicated to prevent cardiac or lipid problems and is not
effective in delaying dementia
2. Osteoporosis prevention or treatment (see Chapter 14)
3. Vaginal atrophy and irritation

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a) OTC lubricants or moisture barriers should be used 2 to 3 times qd
externally
b) topical vaginal estradiol cream can be used in small amounts daily
c) transvaginal estrogen ring (Estring) or Vagifem tablet
d) manual manipulation, either intercourse or digital manipulation, will
increase the elasticity of the vaginal tissue
e) ospemifene (Osphena) 60 mg qd (estrogen receptor modulator) for
dyspareunia secondary to vaginal atrophy
4. Emotional lability and change in sleep patterns may need a
combination of medications to control (see Table 18-1)
a) SSRIs help with emotional symptoms
b) TCA and trazodone may help with sleep disturbances
5. Vasomotor symptoms
a) herbal therapies
(1) black cohosh 20 to 60 mg bid for mood swings, vaginitis, hot flashes
(not to be used with breast cancer)
(2) dong quai 3 caps tid or 3 g raw herb steeped tea 1 to 3 times a day for
hot flashes
(3) evening Primrose oil capsules 2 to 4 caps bid for hot flashes and mood
swings
(4) vitamin E 800 to 1000 IU/day or can be used topically for dry skin
(5) ginseng 100 to 500 mg/day for overall feeling of well being
(6) red clover (Promensil) 40 to 80 mg/day for hot flashes
(7) soy extract caps 50 to 100 mg 2 to 3 times a day for hot flashes
b) conjugated estrogen/bazedoxifene (Duavee) 1 tab qd
c) drug therapies (all off-label use)
(1) venlafaxine 37.5 to 75 mg qd
(2) fluoxetine 10 to 20 mg qd
(3) clonidine 0.1 mg bid to tid
(4) gabapentin 300 mg hs

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6. Testosterone may improve sexual desire (not guaranteed to work);
monitor closely for adverse effects, including deepening of voice,
hirsutism, worsening lipid profiles
7. Various types of topical estrogens, progesterones, and combined oral
products are available (see Table 11-4)
a) can individualize therapy to meet patient’s needs
b) use any estrogen product for the shortest amount of time required to
control the symptoms being treated
c) if the woman has a uterus, also prescribe progesterone
C. Compounding hormone products can help to individualize therapy
1. Estrogen, progesterone, and testosterone can be compounded either
together or separately in oral capsules, creams, patches, vaginal
creams, or troches
2. Common equivalent doses for commercially prepared and
compounded oral estrogens
a) conjugated equine estrogen (CEE) 0.625 mg = oral estradiol 1 mg =
estradiol patch 0.05 mg = biestrogen 1.25 to 2.5 mg bid (compounded
as 80% estriol, 20% estradiol)
b) CEE 1.25 mg = oral estradiol 2 mg = estradiol patch 0.1 mg =
triestrogen 2.5 to 5.0 mg bid (compounded as 80% estriol, 10% estrone,
10% estradiol)
3. add progesterone 100 mg/day with compounded estrogen to protect
the uterus; may help with mood swings, sleep disruption, and hot
flashes
4. methyltestosterone 4 to 6 mg 1 biestrogen compound cream
5. DHEA ovules intravaginally daily may help with vaginal atrophy and
libido
D. Annual physical (e.g., breast and vaginal examinations, mammogram)
is required for patient on HRT; perform routine screening for
cholesterol and colorectal cancer. For Pap smear recommendations, see
Table 11-1.

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 P r a c t i c e Pe a r l s f o r M e n o p a u s a l T h e r a p y

• Exercise: weight-bearing activity 30 min/day 4 to 6 times a week; strength training may help
to maintain agility and muscle mass
• Natural products high in phytoestrogens can relieve some vasomotor symptoms.

• High dietary intake of soy products (beans, soy milk, flour, tofu),
flaxseed (oil, seeds), red clover, alfalfa, celery, parsley, fennel, apples,
nuts, and whole grains
• These products must be consumed daily to get the required estrogen.
• If rash or skin irritation occurs with patch therapy, have the patient use an inhaled
corticosteroid spray on the skin and let it dry before applying the patch; this should
decrease the reaction (spray dries better than OTC steroid creams).
• Topical estrogen therapy (see Table 11-4) can alleviate vaginal dryness and vulvovaginal
irritation.
• If the patient experiences unwanted symptoms with one type of estrogen or progesterone,
switch to another class of drug; dosing is individual: start with the lowest dose and
gradually increase the dose to control symptom(s).
• HRT may cause breast cancer, thromboembolic events, and gall bladder disease; use caution
when prescribing HRT to women at high risk for these conditions.
• Contraindications to HRT: unexplained vaginal bleeding, active or chronic liver disease or
dysfunction, any vascular thrombotic incident or history of varicose veins, cardiac disease or
recent MI, breast cancer
• HRT is indicated for relief of vasomotor-related symptoms on a short-term basis.
• Abrupt cessation of HRT may cause sudden onset of vasomotor symptoms or vaginal
atrophy.

• If the patient is asymptomatic, slowly stop HRT and discuss healthy

behaviors and other nonhormonal therapies to prevent bone loss and
treatment for recurrent vasomotor symptoms.
• Gradual withdrawal is recommended if the patient has been taking
HRT for >6 months.
• If the patient has been taking HRT for >10 years, consider decreasing
the dose or stop the med and evaluate symptoms.
• Recommend herbal products to decrease symptoms.
• Order BMD after the first year of menopause for baseline data and then q2yr; encourage
daily calcium and vitamin D supplements and weight-bearing exercise.
• Concomitant use of GERD medications can cause decreased absorption of oral estrogen

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 products.

• If the woman is having increased menopause symptoms, hold the

GERD product and monitor symptoms.
• Space doses of thyroid medication and estrogen by 12 hours.
Table 11-4
Hormone Replacement Therapy*

Estrogen Only Progesterone Only Combined Estrogen/Progestin

Conjugated estrogen (Premarin) 0.3 Medroxyprogesterone Combined CEE/medroxyprogesterone (Prempro)

mg, 0.45 mg, 0.625 mg, 0.9 mg, 1.25 (Provera, Cycrin) 2.5 mg, 0.625 mg/2.5 mg, 0.625 mg/5 mg, 0.45 mg/1.5 mg, 0.3
mg, 2.5 mg 5.0 mg, 10 mg mg/1.5 mg

Estradiol (Estrace) 0.5 mg, 1 mg, 2 Micronized progesterone Combined CEE/medroxyprogesterone (Premphase)
mg (Prometrium) 100-200 mg 0.625 mg/5 mg (days 1-14 estrogen alone; days 15-28
hs both hormones)

Esterified estrogen (Estratab, Norethindrone (Aygestin, Combined estradiol/norethindrone (Activella) 1

Menest) 0.3 mg, 0.625 mg, 2.5 mg Nor-QD) 2.5 mg, 5 mg, 10 mg/0.5 mg, 0.5 mg/0.1 mg
mg

Estropipate (Ogen) 0.75 mg, 1.5 mg, Progesterone vaginal gel Combined ethinyl estradiol/norethindrone (Femhrt)
3 mg (Crinone) 4%, 8%; use 1 2.5 mcg/0.5 mg, 5 mcg/1 mg
applicator qod

Estrogens conjugated, synthetic Combined cyclic estradiol/norgestimate (Prefest):

(Cenestin) 0.3 mg, 0.625 mg, 0.9 mg, repeating 6 day cycles
1.25 mg

Estradiol transdermal patches: Estradiol/norethindrone (CombiPatch) 0.05/0.14 mg,

Vivelle-Dot, Climara, Alora, 0.05/0.25 mg
Estraderm Estradiol/levonorgestrel patch (Climara Pro) 4.4
Application varies from biweekly to mg/1.39 mg
weekly

Estradiol vaginal ring inserted q90d Esterified estrogen/methyltestosterone

(Estring 2 mg, Femring 0.05, 0.1 mg) (Estratest 1.25 mg/2.5 mg)
(Estratest HS 0.625 mg/1.25 mg)

Estrogen vaginal creams:

Estrace 0.01%
Premarin cream 0.625 mg/g

Estradiol vaginal tablet (Vagifem)

10 mcg

*This list is not all inclusive.

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Breast conditions
I. Nipple discharge

A. Physiologic causes include the following:

1. Pregnancy and lactation or recent lactation (e.g., bilateral clear to straw
colored with early pregnancy)
2. COC use
3. Overstimulation of breasts
4. Cysts (e.g., unilateral discharge, is usually serous to greenish color)
5. Nipple piercing
6. Cloudy/milky appearance may be common in premenopausal women
and is usually bilateral and painless
B. Pharmacologic causes include the following:
1. Estrogen products, herbal products with estrogenic effects
2. Metoclopramide
3. SSRIs, TCAs, haloperidol
C. Pathologic causes include the following:
1. Cancer (e.g., unilateral discharge, usually clear to bloody color)
2. Pituitary lesion
3. Severe head trauma
4. Mastitis (e.g., unilateral purulent discharge)
5. Mammary duct ectasia (e.g., sticky green-black discharge)
D. Signs and symptoms
1. Breast examination for nodules and any changes in the appearance of
breast (e.g., orange peel, dimpling, or swelling)
2. Express discharge from nipples, note color and unilateral or bilateral
discharge
3. Other body systems: skin (e.g., thyroid disorder), weight gain/loss,
liver tenderness

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 E. Diagnostic testing
1. CBC, TSH, prolactin level
2. Express discharge on slide and send for cytology
3. Diagnostic mammogram
F. Treatment
1. Refer to a surgeon for further evaluation
2. If mammogram is normal or fibrocystic disease is noted
a) discourage manual manipulation of breasts
b) follow-up in office q3-6mo until resolved
II. Mastitis

A. Definition: localized painful inflammation of the breast, usually

because of infection or abscess
B. Signs and symptoms
1. Red, hot painful breast that is firm to touch; usually unilateral but can
be bilateral
2. Fever, chills, malaise
3. Pain with nursing and decreased milk production (usually during first
3 months postpartum)
4. In older nonlactating women, usually caused by inflamed milk ducts
near nipples: breast mass near nipples with discharge or enlarged
axillary lymph nodes with nipple retraction
C. Treatment
1. Stop breastfeeding (during infection and antibiotic use) but pump to
express milk routinely until infection clears; consider referral to a
certified lactation specialist
2. Warm, moist compresses 3 to 4 times a day
3. Increase fluid intake and rest
4. NSAIDs or acetaminophen routinely
5. If nonlactating woman, close follow-up for resolution and consider
diagnostic mammogram to rule out inflammatory breast cancer

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 D. Antibiotic therapy for 10 days
1. Dicloxacillin 500 mg qid
2. Cephalexin 500 mg tid
3. Clindamycin 300 mg qid
4. TMP/SMX DS bid
5. Amoxicillin-clavulanate 500 mg bid-tid
E. Consider treatment for candida, especially if the infant has thrush
1. Clotrimazole 1% cream bid or nystatin 100,000 U/g cream to the nipple
area bid-tid
2. Must treat the infant for thrush with 100,000 U/ml 1 ml each side of the
mouth qid until resolved
3. If using bottles or pacifier, these must be thrown away and new ones
used after 48 hours of treatment
F. Follow-up in office in 3 to 5 days
G. Refer to a surgeon if not much improved, especially in nonlactating
woman
III. Breast mass

A. Definition: any mass noted in usually smooth breast tissue

B. Signs and symptoms related to breast examination (upright and
supine exam)
1. Note timing of the mass with regard to the menstrual cycle (if
appropriate)
2. Location of mass in relation to nipples and outer edge of the breast
tissue
3. Size, symmetry, mobility, smoothness, and texture of mass
4. Presence of pain with palpation
5. Nipple appearance and any discharge (note odor, color, and
consistency)
6. Texture of breast tissue
7. Note any axillary or clavicular nodes present

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 C. Diagnostic testing: diagnostic mammogram/ultrasound
D. Treatment
1. Referral to a surgeon if indicated or if symptoms do not resolve
2. If normal mammogram, consider treatment for fibrocystic breast
disease
IV. Fibrocystic breast disease

A. Definition: premenstrual breast tenderness; may be either consistent

or cyclic
B. Signs and symptoms
1. Lumpy breast(s) with nodules of varying sizes and shapes
2. Painful on palpation 1 to 2 weeks before menses and may resolve for 2
weeks after menses finish
C. Diagnostic testing
1. Breast examination (see breast mass examination)
2. Diagnostic mammogram and/or U/S if indicated
3. Refer for diagnostic needle biopsy/draining (if indicated)
D. Treatment
1. Decrease or stop caffeine, tea, chocolate, and nicotine
2. Wear a good supportive bra
3. Apply hot or cold compresses to breast when pain occurs
4. NSAIDs of choice
5. Vitamin E 1000 IU 1 tab qd, vitamin B6: 50 to 100 mg 1 tab qd
6. Evening primrose oil 2 caps bid
7. Chaste berry 175 to 225 mg/day
8. Switch to COCs with lowest estrogenic activity or discontinue use

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Gynecologic conditions
Bacterial vaginitis

I. Definition: normal balance of bacteria in the vagina is disrupted, causing overgrowth of certain
lactobacilli

A. Not considered an STI, but is associated with tampon use, douching,

and multiple sex partners
B. Increases chances of acquiring other STIs
II. Signs and symptoms

A. Foul or fishy smelling vaginal discharge that increases before menses

and after intercourse
B. Thin, gray-white (“spilled milk”) vaginal discharge
C. Itching and burning are rare unless coinfection with another pathogen
III. Diagnostic testing

A. Presence of 3 out of 4 of the following is diagnostic of bacterial

vaginitis (Amsel’s criteria)
1. Copious, thin, grayish-white discharge that coats the vagina
2. Vaginal pH >4.5
3. Positive whiff test (fishy odor of vaginal discharge when 10% KOH is
added to sample)
4. Clue cells on wet prep (there are 20% more clue cells than epithelial
cells)
B. If microscopy unavailable: examination findings plus positive whiff
test and pH >4.5
C. Commercially available DNA probe for diagnosing BV is available
IV. Treatment (if the patient is pregnant refer to GYN)

A. Recommended therapy
1. Metronidazole 500 mg PO bid for 7 days or
2. Metronidazole gel 0.75% intravaginal applicator once qd for 5 days or
3. Clindamycin 2% vaginal cream 1 applicator hs for 7 days

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 B. Alternate therapy
1. Clindamycin 300 mg bid for 7 days or
2. Clindamycin 100 mg vaginal supp hs for 3 days or
3. Tinidazole 1000 mg qd for 5 days or 2000 mg qd for 2 days
C. Recurrent vaginitis therapy
1. Tinidazole 1000 mg qd for 5 days or
2. Metronidazole 500 mg bid for 7 days with
a) intravaginal boric acid 600 mg hs for 21 days
b) if in remission by testing ∼2 days after last boric acid treatment, can
start metronidazole gel 0.75% 2 times a week for 4 to 6 months
3. Intermittent treatment with vaginal metronidazole gel q1wk or 2 g po
q1mo
4. vaginal acidifiers (lactate and acetic acid gels, acidophilus vaginal
suppositories) for symptom relief near menses
5. Intravaginal boric acid 600 mg at hs 1 to 2 times weekly may control
symptoms
6. Betadine gel or compounded vaginal suppository bid for 14 to 28 days
7. treat for any concurrent Candida infection with diflucan 150 mg

P r a c t i c e Pe a r l s f o r B a c t e r i a l Va g i n i t i s

• Avoid douching and use sanitary napkins instead of tampons.

• Limit the number of sexual partners.
• Encourage all-cotton underwear and clothing that is not constrictive.
• Avoid alcohol while taking metronidazole and for 72 hours after finishing medication.
• If using clindamycin vaginally, do not use latex condoms/diaphragms for 5 days
(clindamycin weakens latex).
• No need to treat sexual partner.
• Condoms may reduce the risk of recurrent BV.

Atrophic vaginitis

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I. Definition: inflammation, thinning, and dryness of vagina in postmenopausal women not
using estrogen replacement
II. Signs and symptoms

A. Irritation, burning, and extreme dryness

B. Dyspareunia
C. May have purulent vaginal discharge and odor
D. Vagina is dry and smoother with red epithelium; may see erosions
and fissuring in vaginal walls and introitus
III. Diagnostic testing

A. Wet prep shows few to no lactobacillus and increase in WBCs

B. Yeast and BV are rarely seen
C. If Pap smear done, may show atrophic changes
IV. Treatment

A. Estrogen replacement (see Table 11-4) in any form; topical can be

inserted into the vagina or applied to outer genitalia 1 to 3 times a
week
1. Can use estradiol vaginal ring inserted q3mo
2. Intravaginal estradiol tablet (Vagifem): qd for 2 weeks; use for the
shortest amount of time but may need to use intermittently for
symptom control; if using more consistently, add progesterone if the
uterus is intact
3. Ospemifene (Osphena) 60 mg qd orally
B. Can use moisturizers (e.g., water-based jelly or silicone lotion) 1 to 2
times a day if not interested in estrogen
C. Mixture of equal portions of Vaseline and OTC hydrocortisone cream,
apply in small amounts topically to the vulva every night to relieve
itching; use for 7 days, then stop for 7 days, and can repeat cycle PRN

Vulvovaginal candidiasis (VVC)

I. Definition: overgrowth of normal yeast that occurs in vagina secondary to hormonal

imbalances or changes in vaginal acidity

A. Causes

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 1. Antibiotic therapy
2. Poor control or new diagnosis of DM
3. OCs
II. Signs and symptoms

A. Intense vaginal itching and burning; occasional pain

B. Thick, creamy (“cottage cheese appearing”) vaginal discharge
C. Vulvar erythema
D. Balanitis, urethritis, cutaneous lesions/rash on the penis
III. Diagnostic testing: wet prep with KOH slide shows budding yeast or hyphae
IV. Treatment

A. Clotrimazole 1% cream 1 applicator intravaginally hs for 7 to 14 days

or
B. Terconazole cream 1 applicator intravaginally hs for 3 days or
C. Miconazole 2% cream 1 applicator intravaginally hs for 7 days or
D. Tioconazole 6.5% ointment 1 applicator intravaginally hs once or
E. Fluconazole (Diflucan) 100 to 150 mg once
V. Prevention

A. Wear loose-fitting clothes, all-cotton underwear, avoid panty hose

B. Remove sweaty or wet clothing as soon as possible
C. Avoid bubble baths and harsh or heavily scented soaps in the genital
area
D. If diabetic, maintain tight control of sugars
E. Use probiotics (especially if on antibiotics)

Vulvitis

I. Definition: inflammation or allergic reaction of vulvar tissues, usually as a result of the

following:

A. Too tight clothing, perfumed soaps, vaginal sprays or coloring

B. Wearing wet clothes or “pads” too long
C. Hot tub or pool chemicals

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 D. Progesterone contraceptives (has drying effect on these tissues)
E. Latex allergy from condoms
F. Vulvar cancer
II. Signs and symptoms

A. Severe vulvar and perineal itching and/or burning

B. Excoriations and bleeding may be present
C. Symptoms may be cyclic or daily; may be unilateral or bilateral
D. Scaly, thickened, whitish patches
III. Diagnostic testing: none recommended unless particular lesions (especially unilateral ones)
noted, then biopsy
IV. Treatment

A. Discourage tight constrictive clothing and remove wet clothing or

pads immediately
B. Sitz baths to decrease itching (e.g., vinegar/water, Aveeno baths)
C. Topical estrogen creams (see Table 11-4)
D. Topical OTC hydrocortisone creams
E. Water-based vaginal lubricants/moisturizers

Vulvar vestibulitis/vulvodynia

I. Definition: unexplained vulvar pain accompanied by limitations in daily activities (sometimes

causing disability) and psychogenic distress
II. Signs and symptoms

A. Acute onset, becoming chronic (lasting years)

B. Pain is burning, stinging, irritation to vulva
C. Classic erythema noted at the 5 and 7 o’clock positions on the lower
vestibule
D. Sexual dysfunction
E. May be associated with an infective process in the external genitalia
(pain syndrome is similar to chronic regional pain syndrome)
III. Diagnostic testing

A. Fungal and bacterial cultures

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 B. Wet prep with KOH testing for yeast
C. Biopsy any suspicious lesions
IV. Treatment

A. Yeast
1. Oral fluconazole 150 mg weekly for 2 months and then once every
other week for 2 months
2. Topical nystatin or miconazole or clotrimazole daily until resolved
B. Topical estrogen small amount bid for 4 to 8 weeks
C. Tricyclic agents for 4 to 6 months
1. Amitriptyline 10 mg hs
2. Desipramine 25 mg hs
D. Low-oxalate diet and calcium/vitamin D supplements with each meal
may neutralize oxalates in urine and decrease irritation
E. Short-term corticosteroid (e.g., triamcinolone) to the vulvar area daily
F. Refer to GYN if not improving

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Sexually transmitted diseases
Pelvic inflammatory disease (PID)

I. Definition: inflammatory/infective syndrome that effects organs of reproduction and can affect
surrounding structures

A. Infection usually starts in the vagina and ascends into the uterus and
fallopian tubes
B. Early diagnosis will minimize long-term complications (e.g.,
infertility)
C. Usually caused by untreated or incomplete treatment of gonorrhea,
chlamydia, E. coli, group A streptococci
D. Commonly occurs between 15 and 25 years of age
II. Signs and symptoms

A. Minimum criteria for diagnosis: treat as PID if the woman is sexually

active, no other cause is identified, and she meets these three criteria
1. Lower abdominal tenderness
2. Adnexal tenderness and/or mass
3. Cervical motion tenderness (CMT)
B. Additional criteria
1. Oral temperature >101°F
2. Abnormal cervical or vaginal discharge
3. AUB
4. Dysuria
III. Diagnostic testing

A. Elevated WBC, ESR, C-reactive protein

B. Laboratory documentation of infection with N. gonorrhoeae or C.
trachomatis
C. Transvaginal or pelvic U/S showing thickened, fluid-filled tubes or
free pelvic fluid
D. UCG (do not miss pregnancy)

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IV. Treatment

A. If severe infection (e.g., high fever, N/V) requiring IV antibiotics, refer

to ED
B. Outpatient treatment (oral antibiotics are given for 14 days)
1. Ceftriaxone 250 mg IM once plus doxycycline 100 mg bid with or w/o
metronidazole 500 mg bid (e.g., to treat BV that usually occurs with
infection) or
2. Cefoxitin 2 g IM once plus probenecid 1g once plus doxycycline 100 mg
bid with or w/o metronidazole 500 mg bid
3. If allergy to above: levofloxacin 500 mg qd or ofloxacin 400 mg bid or
moxifloxacin 400 mg qd (caution if <18 years old) with or w/o
metronidazole 500 mg bid
C. Patient should respond to treatment within 72 hours; if improving,
follow-up in 4 to 6 weeks; if worsening, refer for hospitalization
D. Refer
1. To OB if the patient is pregnant
2. To ED if no improvement with outpatient therapy or for severe illness
E. Treat partner empirically
F. Consider HIV testing and counseling

Trichomoniasis vaginitis

I. Definition: infection caused by Trichomonas vaginalis, most common anaerobic, flagellated

protozoan found in the vagina (see Figure 1-8); is considered an STI
II. Signs and symptoms

A. Yellow-green frothy discharge and foul odor

B. Vulvar itching; redness and burning of genitalia
C. Dysuria
D. Dyspareunia and symptoms may increase with intercourse or after
menses
III. Diagnostic testing

A. Wet prep shows trichomonads (see Figure 1-8) and WBC >10/hpf
(may see trichomonads in urine specimen)

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 B. Whiff test may be positive for amine odor
C. pH >4.5
D. Commercial testing with Trichomonas Rapid test of vaginal secretions
IV. Treatment (refer to OB/GYN if pregnant)

A. Metronidazole 2 g in 1 dose or
B. Tinidazole 2 g in 1 dose
C. Alternative dosing: metronidazole 500 mg bid for 7 days
D. Consider betadine or vinegar douche qd for 1 month, recheck after
treatment

Gonorrhea

I. Definition

A. Infection caused by N. gonorrhoeae, involving any mucus membrane

(e.g., commonly genitalia, but also pharynx or eyes); may disseminate
into joints, endocardium, and meninges
B. After exposure, approximately 60% to 90% of women become infected
C. If untreated, approximately 15% will have PID with increased risk of
infertility
II. Signs and symptoms

A. May be asymptomatic in both men and women

B. Men may have dysuria, urinary frequency, and purulent penile
discharge
C. Women may have purulent vaginal discharge with lower abdominal
pain, abnormal menses, and dysuria; pelvic examination: positive
CMT with purulent discharge from the cervix
III. Diagnostic testing

A. Cervical or urethral culture/sensitivity or urine NAAT for GC/CT

B. Consider testing for HIV and other STIs
IV. Treatment

A. Recommended therapy
1. Ceftriaxone 250 mg* IM once plus

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 2. Azithromycin 1 g† once or doxycycline 100 mg† bid for 7 days
B. Alternative therapy
1. Cefoxitin 2 g IM once plus probenecid 1 g once plus azithromycin 1 g
once or
2. Cefoxitin 2 g IM once plus probenecid 1 g once plus doxycycline 100
mg bid for 7 days or
3. Cefixime 400 mg once plus azithromycin 1 g once or doxycycline 100
mg bid for 7 days
C. No sexual intercourse until treatment is completed and symptoms
have resolved
D. When treating, consider chlamydia and treat sexual partners exposed
within the last 60 days
E. No “test of cure” is required; if symptoms do not resolve, obtain
culture
F. Report the infection to the health department

Chlamydia

I. Definition: caused by Chlamydia trachomatis (CT) and is the leading cause of infertility, ectopic
pregnancy, and PID
II. Signs and symptoms

A. May be asymptomatic with mild dyspareunia

B. Mucopurulent cervicitis or vaginal discharge with spotting usually
after intercourse
C. Abdominal or pelvic pain or “heaviness”
D. Pelvic examination: positive CMT with purulent discharge from
cervix; cervix is friable with erosions and irritation
E. Dysuria
III. Diagnostic testing

A. Urine NAAT for GC/CT

B. Culture swab for C/S from cervix or urethra and if indicated, from anal
or oral sites
C. Consider testing for HIV and other STIs

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IV. Treatment

A. Recommended therapy: azithromycin 1 g once or doxycycline 100 mg

bid for 7 days
B. Alternative therapy for 7 days
1. Erythromycin base 500 mg qid (may cause GI upset) or
2. Levofloxacin 500 mg qd (caution if <18 years of age) or
3. Ofloxacin 300 mg bid (caution if <18 years of age)
C. When treating, consider gonorrhea and treat all sexual partners
exposed within the last 60 days
D. Avoid sexual intercourse until therapy is completed (or for 7 days
after single-dose therapy)
E. No “test of cure” is recommended in uncomplicated infection unless
compliance is questioned, symptoms persist, or reinfection is
suspected; return for repeat “test of cure” in 3 months
F. Report the infection to the health department

Syphilis

I. Definition: systemic disease caused by Treponema pallidum

A. Incubation period is 10 to 90 days

B. Recent outbreaks of syphilis have been associated with increases in
HIV infection, drug use, and poverty conditions
II. Signs and symptoms (may occur at any stage up to 30 years after exposure)

A. Primary stage: firm, round, and painless ulcer at site of infection; may
last up to 3 to 6 weeks and then heals without treatment
B. Secondary stage
1. Nonpruritic, rough, red or reddish-brown macular skin rash that
frequently occurs on palms and plantar aspect of feet
2. Lymphadenopathy
3. Arthralgia, malaise, flulike symptoms
4. Anorexia, weight loss
C. Latent/tertiary syphilis is usually asymptomatic for years before

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 symptoms occur and includes progressive neurologic symptoms
1. Dementia
2. Gradual blindness
3. Loss of coordination, paralysis, numbness
III. Diagnostic testing

A. Need to use combination tests to avoid false-positive results: RPR and

VDRL
B. Test for HIV
C. GC/CT culture
D. Hepatitis B and C screen
IV. Treatment

A. Primary stage: benzathine penicillin G 2.4 million U IM in a single

dose; if allergic to PCN, doxycycline 100 mg bid for 14 days
B. Secondary or late stage: referral to an infectious disease specialist
C. Repeat RPR and VDRL testing at 6 and 12 months; if titers are still
elevated, refer to an infectious disease specialist
D. Report the disease to the health department

Herpes genitalis

I. Definition: chronic, life-long viral infection

A. Many people are asymptomatic and unaware of transmission to

others
B. Two types: HSV-1 (usually oral-labial) and HSV-2 (usually genital);
however either one can infect any mucous membrane; virus remains in
the ganglia after infection
C. Recurrent episodes (common) are usually milder and of shorter
duration
D. Possible triggers
1. Stress, illness, fever
2. Menstrual changes, intercourse, trauma
3. Fatigue, poor nutrition

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II. Signs and symptoms

A. May have “flulike” illness with first outbreak along with

lymphadenopathy, watery vaginal discharge
B. Vesicular lesions initially, followed by an ulcerated area on an
erythematous base; vesicles appear “punched-out” on the skin; the
surrounding skin may be spared of redness or swelling (see Color
Plate 20)
C. Pain at site of the lesion with very little itching; prodromal symptoms
may include pain or paresthesias of buttocks, thighs, legs (“boxer
shorts” area)
D. Lesions usually last for about 7 to 10 days
III. Diagnostic testing

A. Lesion: viral culture for herpes and can do reflex for particular type
B. Other STI testing for GC/CT and BV
IV. Treatment

A. Initial outbreak therapy for 7 to 10 days (can be extended if not healed

in 10 days)
1. Acyclovir 400 mg tid or 200 mg 5 times a day or
2. Famciclovir 250 mg tid or
3. Valacyclovir 1 g bid
B. Episodic/recurrent therapy
1. Acyclovir 400 mg tid or 800 mg bid for 5 days or
2. Acyclovir 800 mg tid for 2 days or
3. Famciclovir 125 mg bid for 5 days or 1000 mg bid for 1 day or 500 mg
once, followed by 250 mg bid for 2 days or
4. Valacyclovir 500 mg bid for 3 days or 1 g qd for 5 days
C. Suppressive therapy (e.g., for ≥10 outbreaks/yr) requires daily therapy
1. Acyclovir 400 mg bid or
2. Famciclovir 250 mg bid or
3. Valacyclovir 1 g qd
D. Reevaluate annually and consider providing the patient with refills

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 depending on use to ensure immediate treatment of outbreaks
E. General measures
1. Warm, wet soaks to the genital area using vinegar/water; gently pat
dry the perineal area (do not rub)
2. No feminine hygiene products or douching, no feminine pads; if
concerned about discharge, have extra underwear available
3. Sleep without underwear or clothing in the genital area
4. Wear loose-fitting all-cotton clothing and underwear
5. No intercourse while the lesions are active or any symptoms are
present
6. If symptoms are severe and urination is affected, may need to use
topical xylocaine before urination or may consider intermittent
catheterization for comfort
7. Topical hydrocortisone OTC may help decrease irritation
8. Use condoms for all sexual encounters after symptoms have resolved;
this may decrease the risk of transmission
9. Advise patients that the virus can spread even without the symptoms
being present and that asymptomatic spread is more common in the
first year of infection

Genital warts (condylomata acuminata)

I. Definition: viral lesion caused by human papilloma virus (HPV)

A. Increases risk of vulvar and cervical cancers

B. Most common STI; highly contagious
C. Lesions may occur up to 3 to 6 months after exposure
D. Condoms may decrease the risk but will not be protective because the
virus infects areas not covered by condoms
II. Signs and symptoms

A. May be small, singular or multiple; can have a typical “cauliflower”

appearance or be flat, pedunculated, or rough
B. Warts can be found on the vulva, in the vaginal or anal opening, under
the foreskin of the penis, or on the scrotum; warts may be large

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 enough to limit vaginal, urethral, or anal opening
C. Depending on the size and location, warts can be painful and pruritic
III. Diagnostic testing

A. Usually just visual inspection

B. If no resolution after treatment or worsening with treatment, consider
biopsy
IV. Treatment probably does not eradicate HPV infection but can reduce the size and alleviate
symptoms, with some wart-free periods

A. Warts located on moist surfaces respond best to topical therapies;

therapy may take as long as 3 months to affect lesions
B. Patient-applied therapies
1. Podoflox 0.5% solution or gel
a) apply with a cotton swab to visible warts bid for 3 days, followed by
no therapy for 4 days
b) repeat as necessary up to 4 cycles
2. Imiquimod 5% cream
a) apply at hs 3 times a week for up to 16 weeks
b) wash with soap and water 6 to 10 hours after application
3. Sinecatechins 15% ointment (extract from green tea)
a) apply tid until resolution, but not longer than 16 weeks
b) do not wash off
c) no sexual contact while the ointment is on the skin
C. Provider-applied therapies
1. Cryotherapy with liquid nitrogen q1-2wk
2. Podophyllin resin 10% to 25% in compounded tincture of benzoin
a) the area of application should be small and only on intact lesions
b) apply to each wart and allow to dry before wearing clothes
c) wash off after 1 to 4 hours to reduce irritation
3. Trichloroacetic acid (TCA) or bichloroacetic acid (BCA) 80% to 90%
a) before application, apply a small amount of Vaseline on the

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 surrounding skin to prevent the acid from touching healthy tissue
b) for intense pain, neutralize with soap or sodium bicarb (i.e., baking
soda)
c) repeat treatment q1wk
D. Some lesions will resolve spontaneously
E. Recommend HPV immunizations
1. Gardisil (HPV4) for males and females aged 11 to 26 years; this will be
replaced by HPV9 in the near future
2. Cervarix (HPV2) for females aged 11 to 26 years
F. Refer to a dermatologist or GYN if lesions worsen

*Effective
against conjunctivitis and pharyngitis.
†Effective
against pharyngitis.

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CHAPTER 12

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Common urinary tract conditions
I. The urinary system is responsible for the following:

A. Excretion of waste products of metabolism

B. Maintenance of a constant extracellular environment by balancing
water and electrolytes C. Production of erythropoietin and renin
D. Metabolism of vitamin D to its active form
II. When evaluating the urinary system, the NP should review a urine specimen obtained at the
visit (see Table 4-1)

A. Multi-test stick for abnormality

B. Microscopic evaluation for RBCs, WBCs, bacteria, casts, and crystals C.
Send a portion of the specimen for culture and sensitivity, if indicated
(to identify the causative bacteria and help guide antibiotic use)

P r a c t i c e Pe a r l s f o r U r i n a r y T r a c t C o n d i t i o n s

• Gross hematuria (e.g., pink, red, cola color) and dysuria

• If at the beginning of urine stream, consider urethral dysfunction.

• If at the end of urine stream, consider trigone, bladder, or prostate
cause.
• If throughout voiding, consider renal, ureteral, or bladder pathology.
• If cyclic with menses, consider endometriosis of the urinary tract.
• Microscopic hematuria

• Defined as positive occult blood in two out of three urine samples, with
≥3 RBCs/hpf • Urine should be collected and tested in the same
manner each time.
• Exclude benign causes of microscopic hematuria such as menstruation,
vigorous exercise, sexual activity, viral illness, trauma, or infection.

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• If concerned for primary renal disease because of microscopic hematuria, red cell casts,
proteinuria, and elevated serum creatinine or if the patient’s age is >40 years: obtain renal
U/S and depending on U/S results, consider referral to a nephrologist or urologist for
evaluation.
• If concerned about bladder disease: assess smoking history, irritative voiding symptoms, or
history of recurrent bladder infection; refer for urology consultation.
• Chronic WBCs too numerous to count (TNTC) on repeat UAs with negative culture: check
CBC (if leukocytes >20,000 mm3, consider leukocytic leukemia).
• Elderly patients

• Chronic WBCs under the microscope with few to no signs of UTI

should be evaluated with a catheter specimen; if elevated WBCs are
due to poor midstream UA technique, WBCs will be in the normal
range under a microscope.
• Treatment of asymptomatic bacteriuria leads to antibiotic resistance;
treat only if symptoms are present.
• Consider UTI or sepsis with acute confusion, lethargy, N/V, or
diarrhea; obtain urine specimen as soon as possible.
• In men, 99% of UTIs are due to prostatitis; fluoroquinolones work better than TMP-SMZ and
will need 14 to 28 days of treatment.
• E. coli remains the most common cause of UTI, with the reason being cross contamination
between the anus and urethra (poor hygiene practices or anal sexual practices).
• If complaining of new-onset nocturia: consider polyuria associated with diabetes or HF,
bladder irritability from caffeine or other stimulant drugs, or incomplete emptying caused
by obstruction from a tumor, stool, or an enlarged prostate. Evaluate the problem and treat
as needed.
• Avoid ASA and NSAIDs with renal insufficiency.
• Cystocele grading: first degree, clearly visible; second degree, at introitus; third degree,
protruding from vagina • Preventive measures for acute or chronic UTI:

• Do not douche; this may disrupt normal vaginal flora and encourage
migration of bacteria to the urethral opening.
• Always urinate before and after sexual intercourse to flush harmful
bacteria out of the urethra.
• Do not use bubble baths and perineal sprays; these cause chemical
irritation.
• Wipe the perineum from front to back to prevent the spread of harmful
bacteria.
• Increase fluid intake to 6 to 8 glasses of water a day.

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• Eliminate spermicides, especially nonoxynol-9, which cause irritation
and decrease normal vaginal flora.
• Use cranberry juice or cranberry pills only at bedtime (too much
cranberry can cause overacidification of urine and irritation of the
bladder lining).
• Drinking apple cider vinegar (2 to 4 oz) qd may provide a bactericidal
environment for the bladder.
• Female barrier methods of contraception, such as diaphragms, can
contribute to UTIs; if this is the method of contraception, prophylactic
antibiotics may be needed after intercourse.
• UTI symptoms that are not severe but “bothersome” and are usually present for >2 weeks
and associated with fatigue but without fever may be due to Staphylococcus saprophyticus.

• Urinalysis and microscopy may be unremarkable but urine for culture

and sensitivity will identify the organism.
• Second most common cause of UTI in young sexually active women
• Can be associated with kidney stones, septicemia, and pyelonephritis.
• Usually sensitive to all antibiotics

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Common urinary tract disorders in men and
women
Interstitial cystitis (IC) (synonyms: Urethral syndrome, bladder
pain syndrome)

I. Definition: chronic bladder condition that causes pain, pressure, and discomfort in the bladder
and surrounding structures; associated with urinary frequency or urge to urinate; may be
considered a chronic pain syndrome

A. Suspect IC if the patient has recurrent UTIs that do not respond to

antibiotics and/or overactive bladder symptoms that do not respond to
anticholinergic medications
B. Symptoms are present for >6 weeks with no identified infection or
other cause of pain C. Cause: may never be found but usually there is
some type of event before symptom onset
1. Trauma to pelvis, UTI
2. Other inflammatory/autoimmune/pain conditions (e.g., IBS,
fibromyalgia, chronic pain syndrome) 3. Defect in the bladder
epithelium that allows urine to penetrate the bladder wall
D. Affects women more than men and women are usually between 30 to
45 years of age but can be younger
II. Signs and symptoms

A. Urinary frequency or urgency, hematuria, and nocturia

B. Constant or intermittent pain and pressure from the bladder
C. Bladder pain that worsens as the bladder fills; may feel pain in the
urethra or perineal area D. Women feel pain in the vulva and/or
vagina or suprapubic area with palpation E. Men subjectively feel pain
in the scrotum, testicle, or penis; with digital examination, have pain in
the prostate and over the bladder
III. Aggravating factors related to dysuria/frequency

A. Certain foods/drinks, allergic symptoms

B. Stress
C. Varies with menstrual cycle

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 D. Sexual intercourse
IV. Diagnostic testing

A. Urinalysis with microscopic evaluation (see Table 4-1) B. Urine for

C&S
C. CBC
V. Treatment

A. No cure has been identified; treatment is symptomatic to control pain

with urgency and frequency and to improve quality of life B. Begin
conservative treatment with stress management and heat or ice to the
perineum; avoid triggers and manage constipation (if this is an issue);
biofeedback and acupuncture may help decrease pain and allow the
person some control over the situation C. Tricyclic antidepressants:
amitriptyline at bedtime
1. Increases bladder capacity
2. Reduces pain
3. Decreases frequency, bladder spasms, and nocturia
4. Causes drowsiness and fatigue
D. Antihistamines: patients with IC may have too much histamine in the
bladder
1. Hydroxyzine 10 to 75 mg in the evening
2. Cetirizine 10 mg at hs (causes less drowsiness)
E. Pentosan polysulfate sodium (Elmiron) 100 mg orally tid with water 1
hour before or 2 hours after meals (unknown mechanism of action;
may take several months to see results)
F. Lifestyle changes
1. Decrease intake of alcohol, caffeinated drinks, citrus foods and juices,
high-acid foods, spices, chocolate, and artificial flavorings 2. No
smoking
3. Regular physical exercise and bladder training program that will
gently stretch the bladder wall
G. Referral to a urologist for evaluation and further treatment

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Acute uncomplicated cystitis

I. Signs and symptoms

A. Dysuria, frequency, and urgency

B. Hematuria, nocturia, incontinence in an otherwise continent person C.
Usually afebrile
D. Suprapubic pain, pain in the lower back, and general malaise without
fever E. Elderly patients: consider with somnolence, confusion,
decreased appetite and urine output, change in normal behavior
II. Diagnostic testing (see Table 4-1)

A. Urinalysis with microscopic examination

1. Dipstick results: positive for leukocyte esterase; positive for nitrites
(higher predictability if both esterase and nitrites are positive even
with absence of symptoms); may be positive for blood and/or protein;
pH > 7 (usually) 2. Microscopic examination: positive for bacteria
(graded 1+ to 4+ [4+ is the greatest amount of bacteria]); WBCs >5 to
10/hpf and may be “too numerous to count” (TNTC); RBCs <5/ hpf
(but may be higher); no RBC or WBC casts (these are seen with kidney
involvement only); may see many epithelial cells
B. Urine for C&S considered positive for infection if a single organism is
found
1. Colony count >100,000 CFU/ml in an asymptomatic person
2. Colony count 100 to 100,000 CFU/ml in a symptomatic person
III. Recurrent UTI

A. Repeat dipstick urinalysis and microscopic examination; check for

trichomoniasis, persistent bacteria or blood cells B. If culture was not
done initially, obtain C&S
1. If positive for S. saprophyticus, Proteus, Klebsiella, or E. coli, consider CT
scan to evaluate for kidney stones 2. If positive for S. saprophyticus
a) ask about sexual partners, as this is common in sexually active young
women (although it is not considered an STI) b) commonly occurs in
association with vaginal candidiasis
C. Treatment for uncomplicated UTI: young, non-DM people without
structural defects and/or nonpregnant women experiencing their first

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 or second UTI
1. Preferred therapy
a) TMP-SMZ DS 1 tab bid for 3 days or
b) nitrofurantoin 100 mg 1 tab bid for 5 days or
c) fosfomycin powder 3 g single dose or
d) ciprofloxacin 250 to 500 mg bid for 3 days
2. Alternative therapy (if allergy to above)
a) augmentin 500 mg bid for 3 to 7 days or
b) cefdinir 100 mg bid for 7 days
D. For complicated UTI: people who have experienced >2 to 3 UTIs and
may have structural defects, are elderly, or have other risk factors
1. Ciprofloxacin 250 to 500 mg bid for 7 to 10 days or
2. TMP-SMZ DS 1 tab bid for 7 to 10 days or
3. Ofloxacin 200 mg bid for 10 days or
4. Nitrofurantoin (Macrodantin) 50 mg 1 tab qid for 7 days or
nitrofurantoin (Macrobid) 100 mg bid for 5 to 7 days or 5. Levofloxacin
750 mg qd for 5 days or 250 mg qd for 7 to 10 days
E. Recurrent UTI
1. Give same antibiotic but for longer time period depending on C&S
results 2. Should recheck urinalysis 5 days after the last antibiotic was
taken 3. If symptoms have not resolved with initial antibiotic or
lengthening dosage regimen, consider referral to a urologist
F. Pain relief
1. For adults: phenazopyridine (Pyridium) 100 to 200 mg tid for 3 days 2.
Xylocaine jelly can be applied sparingly to the urethra for pain with
urination in adults or children
G. Prophylactic therapy
1. Daily antibiotic therapy for individuals that have had 2 UTIs in 6
months or 3 UTIs in 12 months
a) nitrofurantoin 50 mg qd or

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 b) ciprofloxacin 250 mg tablet ½ tab qd or
c) TMP-SMZ single strength or DS qd or
d) cephalexin 125 to 250 mg qd
2. Intermittent prophylactic antibiotic taken just after intercourse for
women who have postcoital UTIs secondary to urethral irritation
a) cephalexin 250 to 500 mg or
b) ciprofloxacin 125 mg (1⁄2 tab of 250 mg) or
c) nitrofurantoin 50 to 100 mg or
d) TMP-SMZ single strength or DS
H. Refer to a urologist
1. For a boy after first UTI and girl after second UTI; consider renal
ultrasound and if normal, referral might not be necessary at that time
2. All children with gross hematuria
3. Adults with gross hematuria not cleared with first round of antibiotic
or negative culture 4. All infants aged <3 months with possible UTI should
be transferred to ED

Acute pyelonephritis

I. Signs and symptoms

A. Adults
1. Fever >102°F (fever not always present), chills
2. Flank pain (CVAT) may be severe and is usually over the involved
kidney but can be bilateral
3. N/V, malaise, and anorexia
4. May present with a history of having symptoms for several days
B. Children aged >2 years
1. Unusual odor to urine; hematuria
2. New-onset feeding difficulty; failure to thrive
3. Apathy, irritability, seizures
4. Fever; abdominal or flank pain, or new-onset enuresis

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 C. Infants and children aged <2 years
1. Fever not related to URI or other infection
2. Poor feeding, lethargy, irritability
3. Vomiting, diarrhea, and generalized abdominal pain
4. Hematuria; malodorous urine
5. Jaundice (<3 months of age)
D. Elderly
1. Fever (less common)
2. Mental status changes (common)
3. Generalized deterioration
4. Decompensation in another organ system (e.g., HF)
II. Diagnostic testing

A. Dipstick urinalysis will be positive for leukocyte esterase, nitrites,

blood (either occult or gross), and proteinuria B. Urine microscopic
examination: positive bacteria, WBCs >10 to 20/hpf, RBCs >3/ hpf, and
presence of RBC/WBC casts are suggestive of pyelonephritis C. Obtain
urine for C&S to help guide antibiotic treatment
D. CBC, basic metabolic panel for BUN and creatinine
E. Consider plain abdominal films (may show calculi)
F. Consider renal U/S (may show early scarring)
III. Treatment: consider hospitalization if pregnant, severe nausea/vomiting with dehydration,
and any child aged <2 years IV. Treatment for out-patient therapy

A. IV fluids in office, if available, and then encourage high intake of

water or oral hydration solution (see Table 10-3) at home B. Treat
nausea and vomiting with antiemetics (promethazine or ondansetron)
C. Acetaminophen (no ibuprofen) routinely, depending on age
D. Antibiotics for adults: ceftriaxone 250 to 500 mg IM once, then start
the following:
1. Ciprofloxacin 250 to 750 mg 1 tab bid for 14 days or
2. Ciprofloxacin XR 1000 mg 1 tab daily for 7 days or
3. Levofloxacin 250 to 750 mg 1 tab qd for 10 days or

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 4. TMP-SMZ DS 1 tab bid for 14 days (if the pathogen is known to be
susceptible)
E. Follow-up care
1. Should return to office in 24 hours and 72 hours after treatment
initiated to evaluate progress 2. Repeat urinalysis 3 to 5 days after
antibiotic is completed; if symptoms are not resolving, refer to a
urologist or ED
F. Criteria for referral to a urologist
1. Children aged <2 years
2. Any child with recurrent UTI or pyelonephritis
3. Men with first episode of pyelonephritis (complicated or
uncomplicated) 4. Women with recurrent pyelonephritis

Acute glomerulonephritis

I. Definition: acute infection in kidneys in children and adults; most commonly caused by
Streptococcus; can cause damage to the glomeruli and basement membrane of kidney.
Symptoms usually appear approximately 7 to 10 days after infection.
II. Signs and symptoms

A. Acute-onset oliguria, gross hematuria, possible HTN

B. Edema of hands and face in the morning and feet and ankles in the
evening C. Malaise, lethargy; back pain
D. Weight gain
III. Diagnostic testing

A. Dipstick urinalysis shows hematuria, protein

B. Microscopic examination shows the following:
1. WBCs >10/hpf and RBCs >10/hpf
2. RBC casts, dysmorphic RBCs (irregularly or oddly shaped RBCs from
passage through glomerular structures)
C. CBC (checking for anemia)
D. BMP to check BUN and creatinine, K+, and Na+
E. Renal U/S
IV. Treatment: transfer to ED

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V. Posthospital follow-up

A. Monitor CBC, BMP, U/A

B. Perform 24-hour urine for protein/creatinine q3mos until normal or
stabilized for the patient C. Monitor weight and edema status
D. Monitor BP weekly (or more often if quite elevated)
E. Refer to nephrologist if not improving

Bladder cancer

I. Signs and symptoms

A. Unintentional weight loss

B. Persistent, painless hematuria; suprapubic mass
C. Usually no fever or infection but may have persistent dysuria
D. May see urinary retention or overflow incontinence in a patient who
was previously continent E. Bone pain and anemia (in later stages)
II. Diagnostic testing

A. Urinalysis shows cloudy, concentrated urine

B. Dipstick shows positive hematuria and proteinuria with possible
leukocytes C. Microscopic examination shows RBCs >10/hpf, RBC casts
(no WBC casts), WBCs >2 to 3/hpf D. Consider renal U/S and bladder
U/S
III. Treatment: refer to a urologist; encourage smoking cessation

Renal calculi (kidney stones)

I. Signs and symptoms

A. Pain
1. Sudden onset; described as colicky and severe, intermittent and
paroxysmal 2. Caused by obstruction and not by movement of the stone; if
pain resolves, obstruction has been relieved, but the stone still may be
present 3. Located in the flank and usually related to obstruction in the
upper ureteral or renal pelvic area 4. Males: may radiate to the testicle
(on the same side) and usually related to lower ureteral obstruction 5.
Severe enough that most people cannot find a comfortable position
and will “pace” to help relieve pain; the patient will frequently

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 comment: “this is the worst pain I have ever had!”
B. Gross or microscopic hematuria
C. N/V
D. Dysuria and urgency (frequently caused by obstruction in the distal
ureter)
II. Diagnostic testing

A. Dipstick urinalysis is usually normal except for blood and protein;

microscopic examination shows RBCs >5/hpf B. Noncontrast helical CT
scan (gold standard) for detection of stones and urinary tract
obstruction C. If the stone is obtained, send for analysis to help direct
therapy D. CBC, basic metabolic panel
III. Treatment

A. Urgent referral to ED or urologist if the pain is uncontrollable,

urosepsis is present, unable to keep fluids down, or oliguria/anuria is
present B. Most patients can be conservatively managed with the
following:
1. Pain medications
a) opioids for severe pain
b) NSAIDs (if not contraindicated) will decrease ureteral smooth muscle
tone and alleviate muscle spasm, allowing stone to pass (e.g., ketorolac
10 mg tid day 1, then qd days 2 to 3 if cre <1.6mg/d1)
2. Increase fluid intake to help passage of the stone (stone passage really
depends on the size and location) 3. Use urine strainer for several days
after symptoms and if the stone is obtained, send for analysis
C. Prophylaxis based on dietary modifications and pharmacological
therapy
1. Calcium stones are most common
a) increase fluid intake (e.g., up to 2 L/day) to increase urine flow and
protect against stone formation (dehydration is common cause) b)
increase dietary calcium (but in moderation) and potassium to increase
citrate excretion, but avoid calcium tablet supplementation (this may
increase the risk for further stone formation) c) coffee, tea, and alcohol
may be associated with a lower risk of stone formation d) avoid

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 grapefruit, soft drinks, spinach, rhubarb, peanuts, cashews, and
almonds
e) low sodium diet (80 to 100 mEq/day): Na+ causes the kidneys to
excrete more calcium into urine and high concentrations of calcium in
urine combines with oxalate and phosphorous to form stones f) limit
sucrose and fructose in drinks/foods and limit animal protein g) limit
vitamin C intake; this causes increased oxalate excretion which may ↑
stone formation h) prophylactic pharmacological therapy for calcium
stone
(1) thiazide diuretics (e.g., HCTZ or chlorthalidone) to decrease urinary
calcium (2) potassium citrate (Urocit-K) to increase urine pH
2. Uric acid stone is the only stone that can be dissolved
a) increase fluid intake to 2 L/day
b) potassium citrate (Urocit-K) increases urine pH
c) allopurinol interferes with xanthine conversion to uric acid
3. Cystine stones can be treated with increased fluid intake, urinary
alkalinization, and tiopronin (Thiola)
D. Referral to a urologist if
1. Recurrent renal stones with or without recurrent UTI
2. Ureteral stone >5 mm

Urinary incontinence (UI)

I. Definition: any involuntary loss of urine, which is more common in women and is not related
to spinal cord injury or genitourinary tract trauma II. Use the patient’s history and physical
examination to determine the type of incontinence

A. Stress incontinence is an instantaneous involuntary loss of urine with

any activity that increases intraabdominal pressure, such as physical
exercise, sneezing, or coughing
1. Symptoms are related to weakness of the pelvic floor musculature and
urethral hypermobility
a) usually seen in women aged 19 to 64 years after multiple births
b) some men will experience this after prostate surgery
c) involuntary loss of urine occurs simultaneously with high impact

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 activity and affected individuals are continent for all other activities;
usually continent at night
2. Diagnostic testing
a) urinalysis to rule out infection
b) postvoid residual >100 ml
c) pelvic examination for laxity of muscles and cystocele
d) DRE for sphincter tone
3. Nonpharmacologic treatment
a) timed voiding to avoid full bladder
b) pelvic muscle (Kegel) exercises up to 100 to 200 times qd; start slow
and gradually increase c) change fluid intake pattern to include more
frequent smaller amounts and no beverages before exercise
d) avoid alcohol, caffeine, and smoking
e) weight loss, if indicated
4. Alternative pharmacologic treatment
a) pseudoephedrine HCL 15 to 30 mg before exercise
b) estrogen vaginal cream or Estring
c) vitamin E 800 to 1000 IU qd
5. Refer to a urologist if no improvement
B. Urge incontinence is an involuntary loss of urine that is accompanied by
immediate urgency to urinate without warning; may not get to the
bathroom before leakage occurs
1. Caused by overactive, unstable detrusor muscle; leads to uncontrolled
muscle contractions and can become a social and health problem 2.
Signs and symptoms: dysuria with urinary frequency as often as q1-
2h, nocturia with occasional leakage; may see perineal skin irritation
from urine and from frequent wiping of the perineum 3. Diagnostic
testing
a) urinalysis to rule out infection and glucosuria; consider C&S (catheter
specimen would be more reliable) b) CBC, BMP (looking for elevated
glucose and creatinine)

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c) postvoid residual >100 ml
d) pelvic examination for abnormalities and muscular laxity and for
cystocele e) DRE for impaction and rectal tone (for men, size of
prostate)
f) referral for urodynamic testing to assess bladder function
4. Treatment based on behavior modification therapy
a) spread out daily intake of fluids; refrain from any large intake of fluids
at one time b) avoid or reduce food or beverages that irritate the
bladder, especially tea, caffeine, cola, chocolate, aspartame c) planned
schedule of voiding
d) may need to consider superabsorbent adult diapers or condom
catheters if no control or at bedtime e) when urge is felt, stop and
contract pelvic muscles 2 to 10 times, relax and repeat until the urge
subsides, then proceed to the bathroom f) weight loss, if indicated
5. Treatment based on pharmacologic therapy
a) oxybutynin XL (Ditropan XL) 5 to 30 mg qd or
b) solifenacin (Vesicare) 5 to 10 mg qd (no CNS effects) or
c) tolterodine XR (Detrol XR) 4 mg qd (no CNS or CV effects) or
d) darifenacin (Enablex) 7.5 to 15 mg qd (no CNS or CV effects) or e)
trospium (Sanctura) 20 mg bid or 20 mg hs for age >75 years or f)
trospium XR (Sanctura XR) 60 mg qd (safest for elderly people, no
cognitive impairment) or g) fesoterodine (Toviaz) 4 to 8 mg qd or
h) mirabegron (Myrbetriq) 25-50 mg qd
i) topical estrogen cream
6. Botox injections have been partially successful
7. Referral to a specialist for further treatment modalities and possible
surgery
C. Overflow incontinence (now termed chronic urinary retention) is
involuntary dribbling loss of urine because of overdistended bladder
1. Caused by a dysfunctional detrusor muscle, which causes hypotonia
and lack of contraction, resulting from
a) fecal impaction, holding urine too long

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 b) BPH, B12 deficiency, neurological problems
c) certain medications (e.g., tranquilizers, sedatives, opioids)
2. Signs and symptoms may be very subtle with constant dribbling of
urine, causing body odor and irritation to the perineum 3. Diagnostic
testing
a) urinalysis and possible C&S (catheter specimen is more reliable) b)
CBC, CMP, PSA
c) postvoid residual (will usually see amounts >500 ml)
4. Treatment
a) refer to urologist
b) review current medications and remove causative agents
c) if fecal impaction, remove and start bowel program
d) may need to place an indwelling catheter initially; then begin bladder
retraining and use intermittent catheterization (can teach the patient or
family how to perform) until normal urination is established
D. Transient incontinence is acute onset of involuntary loss of urine in a
previously continent patient, usually owing to a reversible cause. If
this is not treated, however, incontinence may continue.
1. If no reversible cause of incontinence is found, referral to a urologist or
urogynecologist is recommended 2. See Box 12-1 for Common Causes
of Transient Incontinence
Box 12-1

Common Causes of Transient Incontinence

Use the mnemonic DIAPPERS

Delirium or confusional state. Can be caused by any illness; is not a bladder issue.
Infection, urinary (only symptomatic)
Atropic urethritis or vaginitis. Causes inflammation with bladder irritation and uncontrolled
bladder contractions. May benefit from 3 to 6 months of topical estrogen.
Pharmaceutical

• Sedatives or hypnotics, especially long-acting agents

• Loop diuretics

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 • Anticholinergic agents, including antipsychotics, antidepressants,
antihistamines (e.g., diphenhydramine), antiparkinson agents,
antiarrhythmics, antispasmodics, opiates, and antidiarrheals, cause
urinary retention with eventual overflow and stool impaction • α-
Adrenergic agonists and antagonists
• Calcium channel blockers
• Vincristine sulfate
• Caffeine
• NSAIDs cause nocturnal diuresis
Psychological, especially depression (rare)
Excess urine output (e.g., HF, hyperglycemia, SIADH)
Restricted mobility with inability to self-toilet. May be due to limited ROM in joints,
hypotension, spinal stenosis, poor eyesight, fear of falling, or being restrained in chair or
bed.
Stool impaction. Causes excess urinary retention by blocking outlet and worsening overflow
incontinence.
From Resnick, N.M. (1990). Initial evaluation of the incontinent patient. Journal of the American Geriatrics Society, 38(3):311-316.

Overactive bladder syndrome

I. Definition: non-neurogenic overactive bladder syndrome is characterized by urinary urgency,
frequency, and nocturia (usually >3 times at night) with or without urgency incontinence

A. More common in women than men

B. It causes social withdrawal and anxiety when going out of house,
related to “not knowing where the bathroom is”
II. Diagnostic testing

A. Urinalysis, consider C&S

B. CBC and CMP to rule out DM and other causes
C. Postvoid residual status
D. Consider referral for urodynamic testing
III. Treatment

A. There is no known cure and treatment is difficult because the results

are slow; often patients quit therapy because they do not obtain results
quick enough B. Using a bladder diary may help guide therapy and
allow patients to see results that are evident during treatment C.

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 Behavioral modification programs (i.e., bladder training programs and
pelvic floor exercises, biofeedback) to help change voiding habits
D. Treat other illnesses or deficiencies such as dementia, limited mobility
secondary to arthritic changes, obesity, or poor hygiene E.
Pharmacologic treatment includes
1. Antimuscarinic medications (see Urge incontinence) 2. Selective β3-
adrenergic receptor agonist: mirabegron (Myrbetriq) 25 to 50 mg qd
(adjust dose for eGFR <60 mL/min) 3. Oxytrol patch OTC apply 1 patch
2 times a week
F. Alternate therapy
1. Estrogen topical creams
2. Botox and neuromodulators
G. Referral to a urologist if not responsive to treatment

Chronic kidney disease (CKD)

I. Criteria for CKD: symptoms present for ≥3 months, with adverse complications related to
health

A. Kidney damage (albumin excretion >30 mg qd) or

B. Decreased kidney function (eGFR <60 mL/min for ≥3 months) and C.
Other markers for kidney damage evidenced for >3 months
1. Abnormal microscopic urinalysis: urine sediment such as RBC casts
(e.g., glomerulonephritis), WBC casts (e.g., interstitial nephritis), oval
fat bodies or fatty casts (e.g., proteinuric diseases), granular casts, and
renal tubular epithelial cells (e.g., parenchymal diseases)
2. Electrolyte imbalance
3. History of kidney transplant
4. Other known structural abnormalities such as hydronephrosis with
obstruction, renal masses, renal artery stenosis, polycystic kidneys
II. CKD staging to help determine the risk of progression to renal failure and end-stage
cardiovascular disease

A. Stage 1: normal eGFR >90 ml/min

B. Stage 2: eGFR 60 to 89 ml/min; stage 1 and 2 are usually asymptomatic
with some HTN and increase in creatinine

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 1. May see hematuria, proteinuria and anemia
2. MRI or CT of kidneys will show evidence of damage
C. Stage 3a: eGFR 45 to 59 ml/min; may see anemia and osteoporosis
D. Stage 3b: eGFR 30 to 44 ml/min; may see anemia and osteoporosis
E. Stage 4: eGFR 15 to 29 ml/min
1. Monitor weight and serum albumin concentration for effects of
malnutrition 2. Patient will possibly need either peritoneal or
hemodialysis
F. Stage 5: eGFR <15 ml/min; kidney failure, patient will benefit from
either peritoneal or hemodialysis
III. Albuminuria staging can show significant deterioration in kidney function even when eGFR
is still in the normal range

A. Albumin-to-creatinine ratio (ACR) <30 mg/g; normal to mildly

increased ACR or microalbuminuria B. ACR 30 to 299 mg/g;
moderately increased ACR or microalbuminuria
C. ACR >300 mg/g; severely increased ACR or macroalbuminuria
IV. Signs and symptoms in early disease

A. Fatigue, insomnia
B. Nausea, taste disturbance and anorexia
C. Skin pallor, skin excoriation, pruritus, and muscle wasting
D. HTN, edema
E. Do not miss symptoms related to hyperkalemia, pericardial rubs, and
pericarditis
V. Diagnostic testing

A. CBC, CMP, PTH, iron studies, A1c, vitamin D, calcium, and

phosphorus levels B. Urine tests
1. Dipstick urinalysis for protein and also for infection
2. Microscopic examination for RBCs and RBC casts
3. Urine for ACR
4. C&S if indicated
C. CXR

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 D. Renal U/S, CT, or MRI (see Table 4-2)
VI. Treatment in primary practice settings

A. Treatment of reversible causes of kidney disease

1. Aggressive treatment of DM, HTN (start ACE/ARB therapy for kidney
protection); monitor renal function at least q6mo
2. Monitor CBC for anemia annually at stage 3, q6mo at stage 4, and
q3mo at stage 5 (if not seeing nephrologist); “normal” H&H with CKD
is approximately 10/30
a) normochromic/normocytic anemia usually with Fe deficiency
b) oral iron supplement is usually not sufficient; patient often requires IV
replacement; goal is ferritin level >100 ng/mL
c) check B12/folate levels
B. Avoid all medications that effect kidney function and adjust other
drug dosages on the basis of eGFR
C. Stop smoking and drinking alcohol
D. Dietary modification of protein (<1 mg/kg/day) and increase in
vitamin D intake on the basis of lab values
VII. Criteria for referral to a nephrologist

A. eGFR <45 ml/min or decline of 30% in 4 to 6 months without an

obvious reason B. ACR >300 mg/g
C. Hematuria not secondary to urological conditions (e.g., lower UTI,
prostatitis) D. Complications of CKD that are not responding to
treatment or may need more in-depth treatment E. Serum potassium
>5.5 mEq/L
F. Patients aged <18 years
G. Difficult to treat HTN
H. Recurrent kidney stones

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Common genitourinary tract disorders in men
Acute bacterial prostatitis

I. Signs and symptoms

A. Fever, chills
B. Malaise, myalgia
C. Low back, pelvic, or perineal pain; may have referred pain to the end
of penis D. Dysuria, frequency, urgency, and nocturia; recurring UTI
E. Prostate is tender, warm, boggy, and irregular on palpation (do not
massage the prostate, may cause bacteremia)
II. Diagnostic testing

A. Urinalysis with microscopic examination shows WBCs >10/hpf and

positive bacteria B. Urine for C&S
C. Culture any penile secretions to rule out STI
III. Treatment for 14 to 28 days

A. Ciprofloxacin 500 mg q12h or

B. Levofloxacin 500 mg qd or
C. Norfloxacin 400 mg q12h or
D. Doxycycline 100 mg q12h or
E. TMP-SMZ DS 1 bid
IV. Follow-up in 1 to 2 weeks or sooner if symptoms worsen; if symptoms do not improve, refer
to a urologist

Benign prostatic hypertrophy (BPH)

I. Signs and symptoms

A. Difficulty in starting or stopping urine stream

B. Decrease in the force of the stream and postvoid dribbling
C. Nocturia
D. Urge or overflow incontinence
E. DRE to evaluate size, symmetry, and texture of the prostate; the

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 prostate is usually firm and symmetrically enlarged with palpation but
should not be tender (tenderness may indicate prostatitis)
II. Diagnostic testing

A. Urinalysis is usually normal except for pyuria and pH >7

B. Increased postvoid urine >100 ml
C. PSA (may be normal or high)
D. Creatinine (should be normal)
III. Nonpharmacologic treatment

A. Limit fluid intake to frequent smaller amounts and decrease after

evening meal B. Urinate frequently during the day
C. Avoid OTC “cold” preparations (e.g., pseudoephedrine and
antihistamines)
IV. Pharmacologic treatment

A. Alpha-1 blocker (listed below from most side effects to least side
effects)
1. Terazosin (Hytrin) 1 mg qd and can increase up to 10 mg qd or
2. Doxazosin (Cardura) 4 mg qd and can increase up to 8 mg qd or
3. Tamsulosin (Flomax) 0.4 mg qd and can increase up to 0.8 mg qd or 4.
Alfuzosin (Uroxatrol) 10 mg qd or
5. Silodosin (Rapaflo) 8 mg qd orally
B. 5α-Reductase inhibitor
1. Finasteride 5 mg qd or
2. Dutasteride 0.5 mg qd
C. Combination 5α-reductase inhibitor + α1a-adrenergic antagonist:
dutasteride/tamsulosin (Jalyn) 1 cap qd D. Phosphodiesterase
inhibitor: tadalafil (Cialis) 5 mg qd
E. Many of the drugs used to treat BPH are known to lower BP with
position changes; patients should be warned to change positions
slowly F. OTC supplement: Pygeum africanum (African plum tree) or
Saw Palmetto
V. Referral to a urologist if symptoms persist

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Prostate cancer

I. Signs and symptoms

A. Localized nodule and painful prostate

B. Unexplained weight loss
C. UTI and/or urinary obstruction
D. Low back pain and pelvic heaviness
E. Hematuria
F. Anemia, SOB, and bone pain (usually in later stages)
G. Usually a slow-growing cancer; symptoms may remain undetected for
years
II. Diagnostic testing

A. PSA is usually increased

B. Increased alkaline phosphatase
C. Digital rectal examination shows an enlarged, asymmetrical prostate
with palpable nodularity
III. Treatment: referral to a urologist

Epididymitis

I. Signs and symptoms

A. Tenderness on the posterior side of the epididymis with induration

and scrotal pain that may radiate to the groin, with significant swelling
in the scrotum; elevation of scrotum relieves pain B. Urinary
frequency, hematuria, and cloudy urine
C. Urethral discharge
D. Fever and chills
II. Diagnostic testing

A. Urinalysis with microscopic examination shows positive bacteria and

WBCs >10/hpf B. CBC shows elevated WBCs
C. Culture penile secretions for STIs
D. Ultrasound of scrotal contents

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III. Treatment

A. If GC/CT is suspected, treat with azithromycin 1 g once or doxycycline

100 mg bid for 10 days with ceftriaxone 250 mg IM once B. If another
organism is suspected (e.g., E. coli), treat for 10 days with levofloxacin
500 mg qd or ofloxacin 300 mg bid C. Pain management with NSAIDs
and/or acetaminophen
D. Scrotal support
E. Warm-to-hot baths or compresses
F. Follow-up in 48 hours and then again in 1 to 2 weeks; if not
improving, refer to a urologist

Testicular torsion

I. Signs and symptoms

A. Sudden onset of severe scrotal pain

B. The scrotum is enlarged, red, swollen with unilateral testicular pain C.
Testes are noted to be “high” in the scrotal sac because of shortening of
the spermatic cord as it twists (highly sensitive sign for torsion) D. N/V
E. Cremasteric reflex absent on the affected side (99% positive sign for
torsion) F. Prehn’s sign negative (elevation of the scrotum does not
relieve pain)
II. Diagnostic testing

A. Urinalysis will most likely be normal but may show hematuria

B. Emergent referral to ED

Testicular cancer

I. Signs and symptoms

A. The presenting symptom may be gynecomastia with breast nodules

B. Firm, nontender nodule/mass or swelling in the testicle with sensation
of fullness or heaviness; the testicular mass does not transilluminate C.
Unexplained weight loss
II. Diagnostic testing

A. CBC, CMP: consider AFP, beta-hCG, LDH

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 B. Urgent scrotal ultrasound
C. Consider mammogram/breast ultrasound if breast nodules are noted
III. Treatment is referral to a urologist and/or surgeon (do not delay referral, this is usually an
aggressive cancer)

Erectile dysfunction

I. Definition: inability to attain or sustain an erection, even with masturbation, sufficient to

complete sexual intercourse II. Signs and symptoms

A. Cause can be organic, psychogenic, or both. If <40 years of age, the

problem is usually psychogenic; if >40 years, the problem may be
organic.
B. Vascular/neurological
1. Gait disturbances
2. Loss of sensation in the skin in the perineal area
3. Loss of bulbocavernosus reflex testing for sacral nerve damage
(elicited by squeezing the penis to cause reflex contraction of the anal
sphincter) 4. May have decreased or absent femoral or lower extremity
pulses
III. Diagnostic testing

A. Obtain good sexual history that includes psychological problems,

number of partners, past problems with erection, erection on
awakening, past illnesses, past and current medications, and past
trauma B. CBC (looking for anemia)
C. CMP with GGT (look for elevated glucose, creatinine, or liver
enzymes, alcohol use) D. Lipids (penile arteries are small and will be
affected sooner by lipid elevation) E. CRP (e.g., inflammatory
response)
F. Total and free testosterone; TSH, prolactin levels
G. Obtain PSA if >40 years of age
H. Digital rectal examination
I. Postage stamp test
1. Place a roll of stamps around the penis at bedtime; if stamps are
broken apart in the morning, erection occurred 2. High sensitivity for

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 differentiating between organic (inability to have erection) or
psychogenic cause (psychological reason for erectile dysfunction)
IV. Treatment

A. Discourage smoking and alcohol use; aggressive control of HTN, DM,

lipids B. Pharmacologic treatment secondary to the following:
1. Significant decrease in testosterone and hypogonadism: testosterone
replacement can be used (either IM, gel, or transdermal patch) 2.
Depression: treat with an antidepressant that does not have sexual side
effects
a) bupropion 100 mg bid and can increase to tid after 3 days
b) mirtazapine 15 mg/day and can increase gradually q2wk to maximum
of 45 mg/day (caution in elderly people)
C. Pharmacologic treatment for erectile dysfunction
1. If currently taking nitrates or nitric oxide, combination with
phosphodiesterase-5 inhibitors may cause life-threatening hypotension; dose
adjustment is required and may need to be off nitrates for up to 5 days
a) sildenafil (Viagra): start with 25 to 50 mg about 1 hour before sexual
activity; 1 dose per day, maximum dose is 100 mg qd b) tadalafil
(Cialis) 5 to 20 mg ∼30 minutes before sexual activity (do not take
more often than q72h) or 2.5 to 5 mg qd without regard for sexual
activity c) vardenafil (Levitra) 5 to 20 mg 1 hour before sexual activity;
if >65 years of age, start with 5 mg dose; 1 dose per day, maximum
dose is 20 mg
2. OTC supplement: Yohimbine (an α2-adrenergic antagonist touted as
an aphrodisiac) 15 to 30 mg qd
D. Referral to a urologist for more extensive therapies

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CHAPTER 13

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Neurologic conditions
For details regarding in-depth physical and cognitive assessment, see Chapter 1.

Equilibrium disturbances

I. Classification (common causes; not all inclusive)

A. Vertigo: spinning or swaying sensation; perception of movement or

whirling; can be of self or surroundings
1. No hearing loss: benign paroxysmal positional vertigo (BPPV),
vestibular neuritis, head injury
2. Hearing loss: Meniere’s disease, acute labyrinthitis
B. Dizziness: feeling “off-balance,” lightheaded, or unsteady
1. Parkinson’s disease
2. DM neuropathy
3. Eustachian tube dysfunction
4. Depression, anxiety
5. Hypoglycemia
C. Presyncope: sense of impending loss of consciousness
1. Orthostatic hypotension
2. Vasovagal syncope
3. Cardiac arrhythmia
II. Evaluation of “dizziness”

A. History is most important

1. Is it brought about by certain movements (e.g., looking up, turning
over in bed)?
2. Is it accompanied by tinnitus or hearing loss?
3. Is it constant or intermittent?
4. Any changes in gait?

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 5. Any recent trauma?
6. Are there other symptoms (e.g., H/A, N/V, vision changes, weakness)?
7. Any new meds?
B. Examination
1. VS, including postural VS (see Chapter 1, Physical Examination, II)
2. EENT
a) EOMs (also check for nystagmus)
b) ENT: check for nasal/sinus congestion, Eustachian tube dysfunction
c) hearing evaluation (e.g., 2-to 3-foot whisper test, rubbing fingers close
to ear)
d) Rinne and Weber’s tests (see Figure 1-2)
3. CV: listen for the following:
a) heart rhythm and regularity, murmurs
b) carotid bruits
4. Neurological
a) CN (see Table 1-4)
b) DTRs
c) Romberg’s test: the patient will fall toward the affected side with BPPV
III. Syncope

A. Cardiac causes
1. Characteristics
a) sudden onset and resolution; feels fine subsequently
b) may be associated with arrhythmias (i.e., fast [SVT, VT, A-fib] or slow
[third-degree AV block with a rate of <30 bpm]) with or without
palpitations
c) may have a diagnosis or history of aortic stenosis, HF, angina or MI,
aortic aneurysm, or dissection
d) consider with medications such as digitalis, beta-blockers, calcium
channel blockers
2. Possible diagnostic tests

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a) listen for bruits in the neck and abdomen
b) orthostatic VS (see Chapter 1, Physical Examination, II)
c) ECG, holter or event monitor, echocardiogram
d) CXR, carotid Doppler
e) cardiac enzymes, complete metabolic profile, CBC
B. Postural (orthostatic) causes
1. Characteristics
a) often occurs when sitting up from supine position and is preceded by
lightheadedness or dizziness; lying down relieves the symptoms
b) may occur as a side effect of many medications (e.g., alpha-or beta-
blockers, diuretics, nitrates, anticholinergics)
c) may be associated with vomiting, often with diarrhea (dehydration)
d) consider with DM (autonomic failure) or with a history of anemia (GI
bleeding)
2. Possible diagnostic tests
a) orthostatic VS (see Chapter 1, Physical Examination, II)
b) ECG
c) CBC, complete metabolic profile; stool for OB
d) Romberg’s test
C. Vasovagal causes
1. Characteristics
a) gradual onset and resolution; patient may feel horrible for up to 1 to 2
days
b) precipitated by physical or emotional stimuli
c) usually preceded by “vagal” symptoms (e.g., nausea, weakness,
yawning, sweating, blurred vision)
d) usually occurs when standing (i.e., in one place for extended time), but
can occur when sitting and straining (as with defecation)
2. Diagnosed primarily by patient’s history

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 D. Metabolic causes
1. Characteristics
a) onset and resolution usually gradual
b) often associated with lightheadedness and paresthesia
c) may be associated with infrequent eating (low blood sugar)
2. Possible diagnostic tests
a) complete metabolic profile, TSH; consider 2-hour GTT
b) consider CT or MRI of brain (see Table 4-2)
c) may be reproducible with hyperventilation

P r a c t i c e Pe a r l s f o r D i z z i n e s s

• BPPV

• Cause: calcium debris (canaliths) within the inner ear

• Consider BPPV with vertigo lasting <1 minute or occurring with
position changes (e.g., turning over in bed, turning or flexing head);
often occurs first thing in the morning; NO hearing loss or tinnitus.
• Treatment
■ Sleep in a recliner for 48 hours (allows canaliths to “settle down”), limit
movements that cause vertigo.
■ With frequent episodes of vertigo: meclizine 25 to 50 mg q4-6h and
taper slowly
■ Epley’s maneuver (canalith repositioning) by P.T. or modified
maneuver for self-treatment
• Acute vertigo AND hearing loss

• Primary concern is possible acute labyrinthitis (a very serious infection)

or acoustic neuroma; immediately refer to ED.
• Meniere’s disease

• Cause: excess fluid in the inner ear

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• Consider with recurrent attacks of intense vertigo lasting 20 minutes to
24 hours; associated with tinnitus and low-frequency hearing loss and
often with N/V.
• Treatment
■ Sodium intake, <2 g qd (very helpful to most patients)
■ HCTZ 12.5 to 25 mg qd
■ Meclizine 25 to 50 mg q6h prn
■ May need antiemetic (e.g., ondansetron 8 mg q12h prn)
• Syncope and severe lightheadedness can accompany pregnancy; faintness or
lightheadedness may be side effects of many antihypertensive medications.
• Consider cerebellar dysfunction or peripheral neuropathy if the patient complains of
dizziness plus imbalance, clumsiness, or incoordination; check B12 and folate (deficiencies
common with alcoholism) and VDRL or RPR (syphilis).
• Consider carotid sinus hypersensitivity if dizziness or syncope occurs during shaving or
when wearing constrictive collars.
• Referral guidelines

• Emergent transfer to ED
■ New-onset vertigo accompanied by neurological signs/symptoms (e.g.,
diplopia or dysconjugate gaze, limb numbness or weakness, slurred
speech) or acute vertigo with new hearing loss
■ Symptoms suggestive of aortic aneurysm/dissection or MI (see Table 8-
4)
■ Syncope with unstable VS
• Neurologist
■ CNS signs and symptoms
■ Progressive, disabling vertigo or dizziness that is resistant to treatment
■ Patient with BPPV who has neurological signs or does not respond to
therapy
• Cardiologist
■ Any CV-related cause of dizziness not responsive to therapy
■ New-onset murmur (obtain echocardiogram before referral)
• Psychiatrist: comorbid psychiatric disorder (e.g., panic disorder or

468
 depression) that does not respond to reassurance and drug
management

Movement disorders

Seizures

I. Definition: paroxysmal, disorderly discharge of neuronal impulses and spread of these

impulses throughout brain tissues

A. May be an isolated event with or without an obvious precipitating

cause or may be recurrent
B. Epilepsy is diagnosed when seizures recur over a period of time
without obvious precipitating events
II. Classification (Figure 13-1)

469
 FIGURE 13-1 ​Types of Seizures. Source: (Modified from Agins AP: Parent &
Educators’ Drug Reference, Providence, RI, 1999, PRN Press.)

P r a c t i c e Pe a r l s f o r S e i z u r e s

• Consult a physician if seizures are different, new onset, or refractory (i.e., do not respond to
therapy); may co-manage with the physician.
• Treatment is based on the seizure type and tolerability of side effects; monotherapy is the
treatment of choice when possible.

470
 • Never stop anticonvulsants abruptly; wean over 2 to 6 months; if the patient is taking >1
drug, withdraw sequentially, not simultaneously.
• Educate the patient on the importance of medication adherence; many treatment failures are
due to poor compliance.
• Febrile seizures

• Usually occur in children aged 6 months to 6 years and with fever

>101°F (rate of fever increase not a factor)
• Unknown cause; CNS infection/inflammation or systemic problem
should be excluded
• Simple: occurs once in a 24-hour period, lasts <15 minutes with no focal
features; complex: occurs more than once in a 24-hour period, lasts >15
minutes, or has focal features or postictal paresis
• Occurrence does not mean that the affected child has a seizure
disorder/epilepsy.
• Driving restrictions vary from state to state; driving requirements can be found at
www.epilepsyfoundation.org/resources/drivingandtravel.cfm.

Tremors

I. New-onset tremor often warrants referral to a neurologist; the most important diagnostic
distinction is between parkinsonian and essential tremors
II. Action tremors: typically increase with muscle activity and are reduced or absent at rest

A. Physiological
1. Characteristics
a) most evident in hands and fingers; worsen with fine motor tasks
b) little functional impairment
2. Treatment
a) reassure the patient that no disease is present
b) avoid caffeine and other stimulants
c) propranolol 10 to 20 mg tid is sometimes helpful
d) anxiolytics for occasional use in stressful situations
B. Essential
1. Characteristics

471
 a) most evident during use of affected muscles; may involve extremities
(mainly upper) or head/neck and voice
b) may cause significant functional impairment; affects writing skills
c) family history of this disorder
2. Treatment
a) avoid nicotine, caffeine, and other stimulants; worsened by stress,
hypoglycemia, and fatigue
b) propranolol 20 mg tid, increase as needed and tolerated and/or
primidone 12.5 to 25 mg hs and increase to 250 mg qd in divided
doses; giving both medications may be more effective than either alone
c) consider P.T. or O.T. consultation for lifestyle changes needed due to
tremors
III. Resting tremor: typically most noticeable when the involved extremities are at rest and is
relieved or absent during activity

A. Characteristics
1. Most commonly seen with Parkinson’s disease but can occur with
other neurological diseases
2. May be asymmetrical, involving the extremities but not usually the
head/neck (although it can affect the tongue, lips, and chin)
3. Typical movement: alternating forearm pronation and supination or
“pill rolling”
B. Treatment: stop or reduce any drugs that might exacerbate
parkinsonism
C. Refer to a neurologist if Parkinson’s disease is suspected

Idiopathic parkinson’s disease

I. Description: chronic, progressive, neurodegenerative disorder usually diagnosed at or after the

age of 50 years
II. Signs and symptoms

A. Early stages
1. Tremor: observed best in relaxed extremity; usually begins unilaterally
in the finger and thumb (“pill rolling”); stops during voluntary
movement

472
 2. Rigidity: detected earliest in neck muscles; cogwheel rigidity on
passive motion; have the patient stand with arms at sides: when the
examiner twists the patient’s shoulders side to side, the patient’s arms
will not swing freely
3. Bradykinesia: slow, fluid movements; gait disturbances (i.e., shorter,
shuffling steps); difficulty initiating voluntary movements (e.g.,
performing tasks like buttoning clothes, double clicking on a computer
mouse, or standing up from a chair)
B. Later stages
1. Postural instability
2. Akinesia (difficulty initiating movement), rigidity, ataxia, festinating
gait (i.e., quicker, shorter steps like running a race), and stooped
posture
3. Excessive salivation, dysphagia, and constipation
4. Low volume, pitch monotony, and dysarthric speech (difficulty
speaking)
5. Expressionless face and decreased blinking
6. Confusion, hallucinations, and dementia
III. Diagnosis

A. Based on clinical findings; can be confirmed only on autopsy

B. There are no radiology or lab tests for diagnosis
IV. Treatment: Refer to a physician (preferably neurologist) for initial diagnosis; may co-manage
with the physician

Headaches

I. History (pertinent to H/A): most important factor for H/A diagnosis

A. Onset: age at onset and chronic or acute onset; if the patient is >50
years of age and with new onset or change (especially in the temporal
area), check for giant cell (temporal) arteritis
B. Similar H/A before, frequency, and patterns of recurrence and/or
recent changes in H/A
C. Presence/absence of aura and/or prodrome

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 D. Pain intensity: mild, moderate, or severe; crescendo or plateau pain
E. Location: localized or radiating
F. Type of pain: throbbing, burning, aching, pressing
G. Associated symptoms: fever, sinus pain, N/V, lacrimation
H. Neurological symptoms: diplopia, photophobia, ataxia, ptosis,
paresis, tinnitus
I. Triggers of pain
J. Treatments used and how often
K. Recent or past exposure to environmental toxins; recent infection
L. Increase in personal stressors; changes in personal life
M. Family history of H/A
II. Physical examination (suggested steps to R/O organic causes of H/A)

A. Head
1. ENT: look for nasal congestion
2. Teeth: look at teeth and percuss with a tongue depressor
3. Sinus: gently press over the frontomaxillary area of the face and over
mastoid processes and C2; increased pain suggests sinus congestion
4. Eyes: gently press on closed eyes; increased pain may indicate
glaucoma, but other symptoms would be present
5. TMJ: palpate TMJ for pain and crepitus
6. Scalp: inspect and palpate for point tenderness
B. Arteries: palpation and also listen for bruits
1. Tenderness over temporal arteries: if the patient is >50 years of age,
consider temporal arteritis; if younger, consider migraine (if H/A
lasting >24 hours)
2. Carotidynia: tenderness associated with episodic, unilateral H/A
C. Neck
1. Meninges: have the patient touch the chin to the chest (flexes low
cervical spine) and the chin to Adam’s apple (flexes high cervical
spine); if the patient is unable to do these maneuvers, transfer to ED

474
 2. Cervical vertebrae: press on spinous processes; head pain is not
associated with a lesion below C4; cervical spondylosis is usually C5 or
lower
3. Cervical muscles: palpate for muscle pain and tenderness
D. Neurological examination (note if the patient can stand from sitting
without any help)
1. Walking on heels and toes
2. CN examination (see Table 1-4)
3. Tandem gait and Romberg’s test
4. Symmetry on motor, sensory, reflex, and coordination tests (see
Chapter 1, Physical Examination, Neurological System)
5. Fundoscopic examination (transfer to ED with papilledema)
III. Red flag H/A

A. First or new-type or worst-ever H/A (possible intracranial bleeding,

CNS infection)
B. New H/A in patient aged >50 years (possible temporal arteritis, tumor,
or intracranial bleed)
C. Worsening pattern compared with usual H/A (possible mass or
subdural hematoma)
D. Signs/symptoms of systemic illness (e.g., fever, vomiting, nuchal
rigidity [possible CNS infection])
E. H/A with exertion (e.g., cough, sneeze, intercourse [possible increased
intracranial pressure])
F. Focal neurological signs (possible CVA, intracranial aneurysm, mass)
G. Patient taking anticoagulants (possible intracranial bleeding)
H. H/A in children
1. Listen for bruits over the carotid arteries; if asymmetrical or
continuous, transfer immediately to ED
2. If the child has a stiff neck with a severe H/A, transfer immediately to ED
(possible subarachnoid hemorrhage or meningitis)
IV. Diagnostic studies

475
 A. Depending on patient history, consider electrolytes, CBC, TSH and
free T4, UA, ESR, toxicology screen
B. CT or MRI scan (see Table 4-2); CT sufficient in most patients;
performed urgently for patients with the following:
1. Recent change in pattern, frequency, or severity
2. Progressive worsening despite therapy
3. Focal neurological signs
4. Onset of H/A at >50 years of age
V. Classification

A. Cluster
1. Characteristics
a) more common in men than women, usually after 30 years of age,
intermittent episodes of attacks with periods of remission lasting ≥12
months
b) occurs up to 8 times qd; often cyclical, occurring at the same time of
day; lasts 10 minutes to 3 hours
c) pain is exquisitely severe, nonthrobbing, and unilateral in the head
and face with pain in, around, or behind eye
d) may worsen when lying still and is associated with pacing, rocking,
and agitation
e) triggers: ETOH, tobacco, histamines, vasodilators, and seasonal
allergies
2. Associated symptoms: only during attacks and are ipsilateral to pain
a) lacrimation, ptosis, and conjunctival injection
b) nasal congestion and rhinorrhea
c) facial flushes, sweating
3. Treatment
a) CT/MRI with initial attack (see Table 4-2); no labs are helpful
b) abortive
(1) O2 at ≥12 L/min using nonrebreathing mask, for 15 minutes with the
patient sitting upright

476
(2) sumatriptan 6 mg IM or 20 mg intranasal
c) preventative: start ASAP at onset of attack and taper med after
expected duration of episode passes
(1) verapamil 120 mg bid, may increase to tid for >10 days; benefit of
medication usually seen within 2 to 3 weeks (may use prednisone
during the first 2 weeks to help)
(2) prednisone 60 to 100 mg qd for 5 to 14 days; taper by decreasing the
dose 10 mg qd
B. Migraine
1. Characteristics
a) most patients have a family history of H/A; rarely starts after 50 years
of age
b) migraine without aura: at least five H/A meeting the following criteria:
(1) lasts 4 to 72 hours
(2) at least two of the following: unilateral, pulsating, moderate-to-severe
intensity, worsened by routine physical activity
(3) at least one of the following during H/A: nausea, vomiting,
photophobia, phonophobia
(4) H&P and neuro examinations do not suggest underlying organic
disease
c) migraine with aura
(1) attacks include transient, reversible symptoms (aura) that gradually
develop over 5 to 20 minutes and last <60 minutes
(a) visual: flickering lights, spots, lines; loss of vision
(b) sensory: pins and needles, numbness
(c) speech disturbance
(d) brainstem: diplopia, vertigo, tinnitus
(2) has features of migraine without aura, and H/A develops during or
within 60 minutes of aura
2. Treatment
a) abortive

477
(1) usually more effective when taken at onset of H/A
(2) try one medication for at least three H/A before deciding it will not
help
(3) medication options (to avoid medication overuse [rebound] H/A,
limit use to <10 days/mo)
(a) NSAIDs, especially naproxen 500 mg bid prn
(b) Excedrin Migraine 2 tabs
(c) acetaminophen 1000 mg q6h prn
(d) triptans (may repeat dose once in 2 hours if needed)
sumatriptan (Imitrex) 6 mg SQ or 50 to 100 mg PO or nasal spray or
zolmitriptan (Zomig) 2.5 to 5 mg PO or 2.5 mg dissolving wafer or
naratriptan (Amerge) 2.5 mg or
rizatriptan (Maxalt) 10 mg PO or orally dissolving tablet or
almotriptan (Axert) 6.25 to 12.5 mg or
eletriptan hydrobromide (Relpax) 20 to 40 mg
(4) may need medication for nausea (e.g., promethazine, ondansetron)
b) preventative
(1) avoidance of possible triggers (Table 13-1)
(2) consider with H/A >2 days/wk; medication used is based on side
effects, other conditions, and cost
(3) beta-blockers (first line)
(a) propranolol 20 mg bid and titrate to 40 to 160 mg qd
(b) metoprolol 50 mg bid and titrate to 100 to 200 mg qd
(c) timolol 10 mg bid and titrate to 20 to 30 mg qd
(4) anticonvulsants (first line)
(a) topiramate 25 mg qd; may increase by 25 to 50 mg qwk up to 100 mg
bid
(b) valproate 500 to 1500 mg qd (not recommended in women of
childbearing age)

478
(5) antidepressants (second line)
(a) amitriptyline 10 mg hs; titrate to 20 to 50 mg hs
(b) venlafaxine 37.5 mg and titrate to 75 to 150 mg qd
(c) fluoxetine 10 to 20 mg qd
(6) OTC products
(a) butterbur 75 mg bid
(b) magnesium 350 to 1000 mg qd
(c) riboflavin 400 mg qd
(7) menstrual migraines (see Chapter 11, Menstrual Migraines)
C. Tension
1. Characteristics
a) bilateral, nonthrobbing, dull, “tight band” around head
b) mild-to-moderate intensity (not disabling) and can last 30 minutes to 7
days
c) often related to stress or mental tension; not aggravated by physical
exertion
2. Treatment
a) naproxen 500 mg bid or OTC pain reliever with or without caffeine
b) butalbital-acetaminophen-caffeine compound (Esgic Plus, Fioricet) 1
q4h prn (has potential for addiction)
c) consider fluoxetine 20 mg in the morning and cyclobenzaprine 10 mg
at hs
d) lifestyle changes may help: regulation of sleep, exercise, and meals
(e.g., decrease red meat, sugar, and chocolate); stress reduction,
biofeedback, stretching exercises
D. Temporal arteritis
1. Characteristics
a) classical: unilateral temporal area; exquisite tenderness or burning,
throbbing
b) may progressively worsen or wax and wane

479
 c) associated with jaw pain on chewing, fatigue, fever, weight loss; may
have vision loss
d) may have tender, engorged vessels across the forehead and temporal
area
2. Treatment
a) obtain ESR (will be increased)
b) steroids: start once diagnosis is strongly suspected, even before
confirmed; prednisone 40 to 60 mg qd in a single dose for 2 to 4 weeks
c) may need opiates for pain
d) urgent referral to a surgeon for possible biopsy; do not withhold
steroids before biopsy is performed
e) refer to a rheumatologist for further care
Table 13-1
Potential Migraine Triggers

Triggers Avoid or Limit* Allowed

Beverages Red wine, beer Whiskey, scotch, vodka, fruit juices, and sauterne and
Coffee, tea, caffeinated colas Riesling wines

Chocolate or cocoa No more than 1 cup coffee, 2 cups tea, 2 soft drinks qd
Noncola soft drinks, flavored waters, decaffeinated
drinks

Dairy products Milk, buttermilk, cream Low-fat or skim milk

Sour cream, yogurt No more than ½ cup yogurt
Hard (aged) cheeses: cheddar Cottage cheese, cream cheese
Brie, processed cheeses Butter, margarine, cooking oils

Meats/poultry Processed meats: hot dogs, bologna Fresh or frozen meats

Aged, cured, smoked, marinated meats Limit eggs to ≤3/wk
Organ meats: liver

Fish Dried, smoked fish, pickled herring Fresh or frozen fish, canned tuna or salmon

Vegetables Most beans and peas String beans

Onions Asparagus, beets, carrots, spinach, tomatoes, squash,
Pickles, olives, sauerkraut corn, zucchini, broccoli, lettuce, potatoes

Grains, breads, Yeast breads (white), sourdough breads Rice, pasta

cereals Whole wheat and rye breads
English muffins, Melba toast, bagels
Most cereals

Soups Soups containing MSG or yeast Homemade soups

480
 Soups from bouillon cubes

Fruits Citrus fruits, bananas, figs, raisins, papaya, Limit citrus and bananas to ½ to 1 qd
kiwi, plums, pineapples, avocados Apples, prunes, cherries, grapes, apricots, peaches,
pears

Desserts, snack Chocolate Sugar candies

foods Ice cream Sherbet, ices, sorbets
Cookies or cakes made with yeast Cookies or cakes made without yeast
Potato chip products Pretzels
Nuts, seeds Jam, jelly, honey
Peanut butter

Additives MSG (may be in Chinese foods) Salad dressings (in small amounts)
Seasonings and spices White vinegar
Soy sauce

Miscellaneous Oral contraceptives

nonfood triggers Air travel
Stress
Weather (low-pressure system)

*Italicized
foods are the most common triggers. MSG: monosodium glutamate.

P r a c t i c e Pe a r l s f o r H e a d a c h e s

• Inform the patient to treat H/A in early stage so that it will not become disabling.
• A H/A diary can be useful to monitor triggers (also see Table 13-1) and treatment
effectiveness.
• If the complaint is H/A, consider migraine first.
• Patient must stop daily use of analgesics to prevent rebound H/A; overuse of meds for even a
few months can make H/A worse or chronic:

• Medications: butalbital ≥5 days/mo; opiate ≥8 days/mo; triptans,

Excedrin Migraine, or NSAIDs ≥10 days/mo.
• To break the cycle, stop the medicine (may need to wean if using opiate
or butalbital multiple times qd).
• Reinforce to use preventive therapy and to not use acute therapy >2
times a week.
• Menstrual migraines tend to be more severe and less responsive to abortive therapy. They
are not commonly associated with aura.

481
 • When to refer to H/A specialist

• Patient with complex medical or psychiatric conditions (e.g., CV or

renal disease, DM, bipolar disorder)
• If treatment options have not helped

Neuromuscular disorders

I. Multiple sclerosis

A. Signs and symptoms

1. Sensory symptoms present in most patients some time during the
disease: numbness, tingling, “pins and needles,” tightness, coldness, or
sensation of swelling of limbs or trunk; may have intense itching
(especially unilaterally in cervical dermatomes)
2. Pain is common: trigeminal neuralgia, dysesthesia (unpleasant
sensation when touched)
3. Fatigue unrelated to the amount of activity performed; may be
improved by rest
4. Coordination: vertigo, gait imbalance; may have intention tremor in
limbs and head
5. Bowel and bladder dysfunction
B. Treatment: refer to a neurologist; may co-manage care
II. Guillain-Barre syndrome

A. Signs and symptoms

1. Progressive (over approximately 2 weeks), fairly symmetrical muscle
weakness, usually with ascending paralysis; may develop paraplegia
or quadriplegia
2. Acute onset of hyperalgesia or myalgia
B. Treatment: immediate transfer to ED
III. Myasthenia gravis

A. Signs and symptoms

1. Cardinal: fluctuating muscle weakness, often with muscle fatigue;
commonly worse late in the day or after exercise; as the disease
progresses, symptoms are continually present but fluctuate from mild

482
 to severe
2. Dysphagia, jaw fatigue with chewing
3. Ptosis, diplopia
B. Treatment
1. Refer to a neurologist; may co-manage care
2. Emergency transfer to ED for myasthenic crisis (abrupt worsening of
symptoms plus possible HTN, respiratory distress, incontinence)

CNS infections (meningitis)

I. Viral signs and symptoms

A. Fever, H/A (usually severe), nuchal rigidity

B. Drowsiness, fatigue, photophobia
C. May have negative Brudzinski’s and Kernig’s signs (see below)
II. Bacterial signs and symptoms

A. Fever, H/A (usually severe), nuchal rigidity, altered mental status

B. Drowsiness, fatigue, seizure
C. With meningococcus: purpura, red papules; maybe faint pink macules
D. Positive Brudzinski’s and Kernig’s signs (see below)
III. Physical examination signs

A. Brudzinski’s sign: passive flexion of the chin on the chest causes

spontaneous hip flexion
B. Kernig’s sign: positive (abnormal) response is inability or reluctance to
fully extend the leg at the knee with the thigh flexed at the hip to 90
degrees; may be performed with the patient supine or sitting
IV. Treatment: immediate transfer to ED

Focal neurological deficit

I. Description

A. CVA: symptoms last >24 hours

B. TIA: symptoms last <24 hours
II. Signs and symptoms (sudden onset)

483
 A. Carotid circulation
1. Hemianesthesia, hemiplegia, neglect
2. May have aphasia, visual field defects
3. May have H/A, seizures, amnesia, facial paresis
B. Vertebrobasilar circulation
1. Diplopia
2. Vertigo, ataxia
3. Facial paresis
4. Dysphagia, difficulty speaking
III. Common causes

A. Circulatory
1. Ischemic (e.g., atherosclerosis)
2. Hemorrhagic (e.g., aneurysm, artery dissection)
B. Embolism related to the following:
1. Mitral valve disease
2. Decreased ventricle wall movement (e.g., with MI or HF) with mural
thrombus
3. Arrhythmia (e.g., atrial fib)
C. Hypercoagulable states, including use of OCs
IV. Treatment

A. Depending on the patient’s condition: emergency transfer to ED

B. Counsel for lifestyle changes (at follow-up visits)
1. Stop smoking
2. Control risk factors (e.g., HTN, DM, hyperlipidemia)
V. Bell’s palsy

A. Acute paralysis of the facial nerve; of unknown cause (possibly herpes

simplex or zoster infection)
B. Signs and symptoms
1. Sudden onset (over hours) of unilateral facial paralysis, including

484
 eyebrow sagging, inability to close the eye, and mouth asymmetry
2. May have decreased tearing and/or loss of taste on the anterior two
thirds of the tongue; no real sensory loss on the face, may have tingling
sensation
3. Progressive course with maximal effects ≤3 weeks from the first day of
weakness (diagnosis is doubtful if no function has returned within 3 to
4 months)
C. Diagnostic tests
1. Sparing of the forehead muscles usually occurs with Bell’s palsy but
this does not exclude a more serious problem
2. Consider CT/MRI (see Table 4-2) with atypical signs if there is
progression after 3 weeks or if there is no improvement at 4 months
D. Treatment
1. Prednisone 60 mg qd for 5 days, then taper off by 10 mg qd
2. Consider valacyclovir 1000 mg tid for 1 week in addition to prednisone
with severe facial palsy (disfiguring asymmetry with little or no
motion in the affected side, incomplete closure of eye)
3. Eye care
a) artificial tears q1h while awake and lubricating ophthalmic ointment
at hs
b) use protective glasses or goggles; patches can be used, but do not
place tape on the eyelid since the patch could slip and abrade the
cornea
E. Refer to a neurologist if continues to progress after 3 weeks or no
improvement by 4 months

485
CHAPTER 14

486
Musculoskeletal conditions
History

I. A chief complaint ascribed by the patient to a joint may originate elsewhere. Bones and joints
can be affected by systemic diseases as well as by local problems.
II. Elicit all factors of the chief complaint and associated symptoms and obtain a careful review of
systems
III. One of the most important points is to determine whether the symptoms are due to structural
damage or inflammatory joint disease (Table 14-1)
Table 14-1
Comparison of Structural and Inflammatory Joint Conditions

Structural Lesion Inflammatory Joint Disease

Pain occurs on use, improves with rest Morning stiffness, especially for >30 min
Usually involves weight-bearing joints Also involves non–weight-bearing joints
No acute exacerbations Often has flare-ups
No systemic symptoms Systemic symptoms common

P r a c t i c e Pe a r l s f o r M u s c u l o s k e l e t a l C o m p l a i n t s

• Pain without injury: consider arthritis (see Common Painful Joint Disorders, later in this
chapter), infection, or metastatic cancer (primarily in the spine and/or ribs)
• Absence of pain in the presence of obvious joint disease: consider neuropathy
• Limp with pain: consider neuromuscular involvement; without pain: consider muscle
disease
• Fatigue and malaise (Table 14-2)
Table 14-2
Possible Causes of Fatigue and Malaise

Associated Symptoms Possible Diagnosis Diagnostic Tests

Fever, lymphadenopathy, weight Malignancy CBC, ESR
loss Possibly CXR, CT, or MRI (see Table 4-2)

Increasing fatigue over time Malignancy or anemia CBC, ESR, chemistry profile
Probably CXR

Possibly CT or MRI (see Table 4-2)

487
 Daytime somnolence, snoring Sleep apnea Sleep studies
(especially if increased), obesity

Flat affect, appetite or sleep Depression None, if no other history findings suggest a
changes, possibly sexual physical cause
dysfunction

Change in skin or hair texture, heat Thyroid disorder TSH and free T4
or cold intolerance, weight changes

Fever, cough; sometimes sore Infection Treat empirically or obtain lab work and x-rays as
throat and lymphadenopathy indicated (e.g., CBC, strep screen, Monospot, CXR)

Weight loss but no fever or Malignancy, poor CBC, chemistry panel

signs/symptoms of infection nutrition, malabsorption Consider x-rays
syndromes

Pallor Anemia See Anemia (Chapter 9)

Stools for occult blood if indicated

Weight loss, polydipsia, polyuria Diabetes mellitus FBG (usually with a chemistry panel)
Possibly A1c

• Paired joints usually provide a comparison, and both should be examined; perform
thorough assessment above and below the area of complaint.
• Remember that joint pain may be referred or radicular (resulting from nerve compression or
injury).
• Inspection and palpation are the primary assessment techniques; percussion is occasionally
used to elicit point tenderness, which may indicate a fracture.
• Ask the patient to touch with one finger the spot that hurts the most (localizes the problem
and helps narrow possible diagnoses).
• Knowledge of surface anatomy is critical to musculoskeletal examination; dermatomes are
illustrated in Figure 14-1.

488
 FIGURE 14-1 Dermatomes. Source: (From Nagelhout JJ, Plaus K: Nurse Anesthesia,
ed 5, St. Louis, 2014, Elsevier.)

• Without appropriate findings for arthralgias/myalgias, there is no need to test for Lyme
disease unless there is a history of exposure or visit to an endemic area.
• Evaluate muscle strength on a scale of 0 to 5 (Table 14-3).

Table 14-3
Evaluating Muscle Strength

Score Description
5 (normal) Has complete joint ROM with full or normal resistance
4 (good) Has complete joint ROM with some resistance
3 (fair) Has complete joint ROM against gravity
2 (poor) Has complete passive joint ROM
1 (trace) Has muscle contraction but limited or no joint motion
0 (none) Has no evidence of muscle function

489
Location-specific musculoskeletal disorders
Neck

I. Inspection: observe for any deformities and abnormal posture

II. Palpation: assess for tenderness and/or muscle spasm

A. Cervical spine processes (Figure 14-2)

B. Trapezius and sternocleidomastoid muscles
C. Muscles between scapulae
III. Muscle testing

A. ROM: Ask the patient to perform the following:

1. Touch the chin to the chest (flexion); abnormal if <60 degrees
2. Touch the chin to each shoulder (rotation); abnormal if <90 degrees
3. Touch each ear to the respective shoulder without raising the shoulder
(lateral bending); abnormal if <45 degrees
4. Tip the head back and look toward the ceiling (hyperextension);
abnormal if <75 degrees
B. Spurling’s maneuver (may be called “axial compression”): patient
seated with head rotated slightly to one side and chin flexed toward
the chest; the examiner presses gently down on the head; if the patient
tolerates this well, repeat with the head rotated slightly to the side and
have him/her look up. Positive test with radicular symptoms beyond
the shoulder: ipsilateral side—consider compression; contralateral side
—consider muscle tension. Perform this on the unaffected side first
and then on the affected side.
C. Assess for bilateral shoulder shrugs (against resistance) and grip
strength
IV. Sensory testing of C-spine (see also DTRs and Figure 14-1)

A. C4-C5: numbness in the deltoid region and diminished biceps reflex

B. C5-C6: numbness in the dorsolateral areas of the thumb and index
finger; diminished biceps and brachioradialis reflexes
C. C6-C7: numbness in the index and middle fingers and back of the

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 hand; diminished triceps reflex

FIGURE 14-2 Upper Spine and Landmarks.

P r a c t i c e Pe a r l s f o r N e c k Pa i n

• Pain not caused by injury and not relieved by rest or is progressive: consider cancer or
infection
• No treatment has been shown to change the natural course of mechanical neck pain;
management is toward patient comfort until it resolves.
• Possible causes of referred neck pain (i.e., absence of physical findings, including neck
tenderness, loss of motion, or pain with motion) include the following:

• Shoulder (bursitis, tendinitis, arthritis)

• Reflex sympathetic dystrophy
• Thoracic outlet syndrome
• Bronchogenic cancer
• CAD, aortic dissection

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 • Peptic ulcer disease, pancreatitis, cholecystitis
• Possible neck pain diagnosis (Table 14-4)

Table 14-4
Neck Pain

Possible
Finding Additional Points
Cause(s)
Acute pain with neck movement, localized and episodic; often Neck Pain relief with relative rest, NSAIDs
present when waking and usually lasts 1-4 days. There is sprain or acetaminophen, muscle relaxers, and
muscle tenderness. hot and/or cold packs
If neck tenderness persists and is
associated with other tender areas in
the body, consider fibromyalgia

Involuntary rotation or lateral bending of the head; usually Torticollis May be acute or chronic
associated with tender muscle spasm, pain with neck
movement, and limited ROM

Acute or recurrent pain, more severe and lasts longer than a stiff Cervical Neurological examination of the upper
neck; may be associated with whiplash injury or sudden strain extremities is normal; if related to
movement; symptoms increase with ipsilateral rotation and trauma or an accident, obtain C-spine
contralateral bending of the neck. May have limited ROM. x-ray with oblique view and refer to or
consult a physician.

Neck pain with radiation: pain similar to cervical strain but with Herniated Refer
sharp, burning, or tingling pain to the shoulder, back, or arm(s). cervical
May have muscle tenderness and/or spasm, limited ROM, and disc
extremity weakness. DJD with
a bone
spur

Shoulder pain
I. With shoulder pain, attempt to answer the following questions:

A. Is ROM normal or abnormal? Is it painful?

B. Are any structures tender (Figure 14-3) and does palpation reproduce
the pain?
C. Is neurological examination of the arm and shoulder normal?
II. Inspection for swelling, deformity, inequality, and muscle atrophy

A. Anteriorly: shoulders (including shoulder height) and shoulder girdle

B. Posteriorly: scapula and related structures
III. Palpation for tenderness and crepitus

A. Site where the patient locates pain

B. Sternoclavicular joint

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 C. Acromioclavicular joint: consider AC joint strain or osteoarthritis
D. Subacromial area (between the humeral greater tubercle and the
acromion process)
IV. Muscle testing

A. ROM (designate by degrees): examine the patient from behind and

ask the patient to perform the following:
1. Raise arms forward and then overhead with palms touching
(elevation, flexion)
2. Keep elbows at the side, swing forearms out: perform with and
without resistance
3. Place each thumb between scapulae: “back scratcher” (adduction,
extension, internal rotation)
B. Muscle strength
1. Have the patient flex the elbow to 90 degrees, then abduct the arm to
90 degrees; have the patient resist as you press down on the distal arm
(evaluates deltoid and rotator cuff)
2. Raise arms straight out to the side (abduction, extension) with thumbs
up and then rotate thumbs down (evaluates rotator cuff): perform with
and without resistance
3. Flex the elbow to 90 degrees while you support the elbow; have the
patient resist as you press against the distal forearm, attempting to
internally rotate the arm (evaluates rotator cuff)
C. ROM testing results
1. ROM full, symmetric, and painless: check for referred pain (Table 14-5)
2. Active ROM is painful or impaired: perform passive ROM. If passive
ROM is normal with abnormal active ROM, it is probably
muscle/tendon weakness or neurogenic weakness; the most common
causes are rotator cuff tear and cervical spine disorders causing deltoid
weakness.
3. Active and passive ROM both limited: try to localize the restriction.
Restrict scapula movement by placing the heel of your hand over the
upper scapula and your fingers over the shoulder; feel the shoulder as
active or passive abduction of the arm is attempted.

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 a) restriction seems inflexible: bony (e.g., degenerative joint disease)
b) restriction “gives away” with pressure and is due more to pain and
muscle spasm: periarticular (e.g., tendinitis, bursitis, muscle spasm or
strain)
D. Determine what degree of shoulder motion causes pain or limitation
(Figure 14-4)
1. All directions of movement: glenohumeral joint itself (e.g., arthritis of
the joint)
2. Initial 30 degrees of abduction impaired: rotator cuff muscles
3. Initial 90 degrees of abduction impaired, but 90 degrees to 180 degrees
normal: rotator cuff muscles, tendons, or bursae
4. Initial 90 degrees of abduction normal, but 90 degrees to 180 degrees
impaired: AC joint disorders
5. Internal and external rotation impaired: rotator cuff muscles, other
muscle spasm, impingement syndrome (most common cause of
shoulder pain)
V. Sensory testing

A. ROM of neck
B. Muscle testing
1. Shoulder shrug against resistance (cranial nerve XI or cervical [C]
nerves 3-5)
2. Scapular retraction: “stand at attention” against resistance (C5)
3. Motor strength of biceps, triceps, and wrist extensors and flexors (see
Table 14-3)
4. Deep tendon reflexes: biceps, brachioradialis, triceps
5. Sensory examination using light touch along dermatomes and
peripheral nerves (see Figure 14-1 for dermatome distribution)
VI. Elevated arm stress test (EAST) for thoracic outlet syndrome

A. Patient stands with the back to a wall and abducts both arms at least
90 degrees and then opens and closes fists at a moderate speed for 3
minutes
B. Results

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 1. Positive test: reproduction of neurological and/or vascular symptoms
2. Negative/inconclusive test: only a sense of fatigue in the arm
VII. Treatment of common shoulder problems

A. Rotator cuff tendinitis

1. Treat with rest and ice for acute pain; may take NSAIDs at full strength
for 3 to 4 weeks
2. Restrict overhead reaching, any movement with the elbow away from
the body, and sleeping on the involved side
3. Once pain has improved, begin gentle ROM movements of the
shoulder; perform to “stretch” and not pain
4. Discourage use of a sling, which may hasten development of a frozen
shoulder
5. Refer if no improvement after 3 weeks
B. Rotator cuff tear: refer to an orthopedic surgeon
C. AC strain
1. The goal is to allow ligaments to reattach
2. Activity limited for 30 days
a) avoid sleeping on either side
b) do not reach overhead or across the chest
c) lift close to the body, but do not lift more than 20 lbs
3. Apply ice (see RICE mnemonic, Table 14-13)
4. Shoulder immobilizer, probably for 3 to 4 weeks
5. If no improvement in 2 weeks, consult or refer to a physician
6. Patient education: if treatment recommendations are ignored, the
ligament may not reattach, leading to persistent symptoms
D. Thoracic outlet syndrome: refer to a physician if suspected

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 FIGURE 14-3 Anatomy of Shoulder. Source: (From Pfenninger JL, Fowler GC:
Pfenninger and Fowler’s Procedures for Primary Care, ed 3, Philadelphia, 2011, Elsevier.)

FIGURE 14-4 Shoulder ROM.

Table 14-5
Referred Shoulder Pain

Site Possible Causes Additional Points

Trapezius ridge Diaphragmatic Perform cardiorespiratory
Pleuritis and abdominal
examinations
Pericarditis

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 Subdiaphragmatic disease Check for postural
hypotension
Ruptured organ (e.g., ulcer)
Ectopic pregnancy
Splenic rupture

Acromioclavicular area Diaphragmatic or

subdiaphragmatic disease (e.g.,
cholecystitis)

Lower scapula Gallbladder disease Check Murphy’s sign (see

Chapter 10, Abdominal
Pain, V, E, 8)

Back of the neck, Cervical spine disease (most Perform neck examination
interscapular area, and common site for referred pain)
posterior shoulder

Deltoid area Articular and periarticular

disorders of the shoulder (e.g.,
arthritis, bursitis)

Mid-humerus (brachial Rotator cuff problem

insertion site)

P r a c t i c e Pe a r l s f o r S h o u l d e r C o n d i t i o n s

• Acute symptoms for <2 weeks: often an injury such as a fracture, rotator cuff tear, or biceps
tendon rupture.
• Night pain is often worse with bursitis and rotator cuff inflammation.
• With burning, constant pain: consider a neurogenic cause.
• Bilateral shoulder pain after 50 years of age: consider polymyalgia rheumatica.
• If considering an MRI or CT, refer to an orthopedic surgeon.
• Common chronic shoulder pain

• Pain on top of the shoulder and worsened by touching the opposite

shoulder with the hand of the affected side: consider AC joint arthritis
or separation
• Pain in the lateral deltoid area and worsened by overhead activities:
consider bursitis, frozen shoulder, or rotator cuff problem

497
 • Shoulder pain relieved by placing the forearm on top of the head:
consider cervical nerve root problem
• Pain along glenohumeral joint lines: consider degenerative arthritis of
the joint
• Aching pain and paresthesias radiating from the neck to the shoulder
and/or down to the hand, associated with intermittent swelling and
discoloration of the arm and worsened by overhead activities: consider
thoracic outlet syndrome
• If the condition does not respond to nonsurgical therapies after 3 weeks, refer to an
orthopedic surgeon.
• See Table 14-5 for referred shoulder pain.

Elbow

I. Inspect and palpate

A. For nodules, swelling, or tenderness of extensor surface of the ulna,

lateral and medial epicondyles, and olecranon process (including the
groove on each side)
B. For muscle wasting of interossei and hypothenar iminence
II. Muscle testing

A. ROM: ask the patient to perform the following:

1. Bend and straighten elbows; if checking ROM against resistance, the
examiner applies resistance at the wrist, not the hand
2. Rest arms at the side with the elbows flexed, then pronate and
supinate the hands with and without resistance (Figure 14-5)
3. Flex the elbows and rest the forearm on a flat surface; have the patient
resist wrist flexion and extension
B. Determine what type of elbow motion causes pain or limitation
1. With flexion/extension: consider ulnar-humeral joint problem
2. With forearm pronation/supination: consider problem with the
proximal radial and/or ulnar joints (e.g., “tennis elbow”)
III. Sensory testing

A. Tinel’s test (for cubital tunnel syndrome): firmly percuss over the
ulnar nerve in the ulnar groove at the palm and elbow; positive test

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 with paresthesias in the ring and little fingers
B. sensation in all finger tips and radial and ulnar sides of hands, front
and back
C. If the pain history indicates a radicular source (e.g., tingling,
numbness), examine the cervical spine (see Neck examination)
IV. Common elbow disorders: see Table 14-6

FIGURE 14-5 Elbow ROM Test.

Table 14-6
Common Elbow Disorders

Possible
Finding Additional Points
Cause(s)
Swelling over the olecranon (can move Olecranon Pull-on elbow brace may help
without difficulty and is not painful) bursitis Aspiration of the bursa for specific diagnosis and then apply a
fairly tight neoprene sleeve and/or consider consultation with a
physician
Often recurs

Pain or tenderness over the lateral Epicondylitis Caused and aggravated by hand and wrist movements; splint
epicondyle, aggravated by resisting (“tennis the wrist to prevent movement and take NSAIDs for 7-10 days
wrist extension elbow”) A tennis elbow band may prevent recurrence
Modify or eliminate causative activities

499
 Pain or tenderness over the medial Epicondylitis Caused and aggravated by hand and wrist movements; splint
epicondyle, aggravated by resisting (“golfer’s the wrist to prevent movement and take NSAIDs for 7-10 days
wrist extension elbow”) Modify or eliminate causative activities

Pain in the elbow and limited ROM Nurse maid’s Refer

elbow
Dislocation

P r a c t i c e Pe a r l s f o r E l b o w Pa i n

• Acute pain

• After injury: consider fracture, dislocation, or tendon/ligament rupture

• Conditions within the joint may cause acute synovitis (e.g., swelling,
tenderness, limited motion): consider septic arthritis (especially with
IV drug abusers), RA, or gout.
• Chronic pain

• Commonly associated with overuse injuries (work or sport)

• May be OA or inflammatory condition (i.e., RA or gout)
• If pain persists despite treatment: consider x-rays, P.T. evaluation,
orthopedic referral.
• A patient with an elbow overuse injury frequently also has rotator cuff tendinitis.
• Referred pain can be from the following:

• Angina
• Cervical radiculopathy
• Carpal tunnel syndrome

WRIST and hand

I. Inspection

A. Inspect for swelling, redness, nodules, deformity, and muscle/thenar

atrophy
B. Have the patient make a fist and look at the knuckle (MCP) profile for
symmetry

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 C. Inspect nails for pitting and other signs of systemic disease
II. Palpation of the following for swelling, bogginess, or tenderness

A. Medial and lateral aspects of each DIP and PIP joint (Figure 14-6)
B. MCP joints just distal to and on each side of the knuckle (use your
thumbs for examination)
C. Wrist joint (your thumbs on the dorsal side and your fingers beneath
it)
D. Capillary refill and radial and ulnar artery pulses
III. Muscle testing (take into account the dominant hand)

A. ROM: ask the patient to perform the following:

1. Make a fist, with the thumb across the knuckles
2. Extend and spread fingers 3 times
3. Touch each finger with the thumb of the same hand (thumb-finger
opposition)
4. With palms down, move the fingers laterally (ulnar deviation) and
medially (radial deviation)
5. Flex and extend wrists with and without resistance
B. Assess grip strength bilaterally (see Table 14-3)
C. Finkelstein’s test for de Quervain’s tenosynovitis: the thumb is held in
the palm with a closed grip; the wrist is passively ulnarly deviated; a
positive (abnormal) result is pain from the radial styloid to the “snuff
box”
IV. Sensory testing

A. For carpal tunnel syndrome (CTS)

1. Phalen’s maneuver: have the patient press the backs of hands together
(flexes wrists at 90 degrees) for 60 seconds; positive (abnormal) results
are numbness and tingling in the thumb and first two fingers
2. Tinel’s sign: hyperextend the wrist and firmly percuss over the median
nerve on the palmar side approximately 1 cm proximal to the wrist;
positive (abnormal) results are tingling or shocklike sensations across
the palm, thumb, and first two fingers
B. Remember that hand or wrist pain may be referred from cervical

501
 nerve roots, brachial plexus, or peripheral nerves; “radicular,” or nerve
pain, is often described as tingling, burning, or numbness and follows
dermatomes (see Figure 14-1) or peripheral nerve distributions; if such
pain is present, check DTRs and sensory status; the following sensory
areas are to be tested:
1. Tip of the index finger (median nerve)
2. Tip of the little finger (ulnar nerve)
3. Dorsal first web of fingers (radial nerve)
4. Dorsal-ulnar surface of the hand (dorsal branch of the ulnar nerve)
V. Common wrist and hand conditions: see Table 14-7

FIGURE 14-6 Anatomy of Hand.

Table 14-7
Common Hand and Wrist Disorders

Finding Possible Cause(s) Additional Points

Hand or finger swelling, pain, or OA or RA, gout See Common Painful Joint Disorders, later in this chapter
deformities Trauma Consider x-rays

Thenar atrophy Carpal tunnel Refer to an orthopedic or hand surgeon

syndrome

Painless swelling (cyst) on the Ganglion No treatment necessary unless painful; may attempt
dorsum of the hand or wrist aspiration with an 18-g needle, compressing cyst as it gets
smaller

Pale fingers and slow capillary Raynaud’s See Chapter 9, PAD, III

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refill phenomenon Consult or refer immediately to the ED if the problem is
Ulnar or radial artery acute
lesion

Loss of resistance against extension Cervical nerve root Refer to a spine specialist or neuro
or flexion lesion

Passive ROM normal with absent Peripheral nerve lesion Refer

active ROM; may or may not have (e.g., radial, median,
pain ulnar)
Brachial plexus lesion

Unable to flex the DIP or PIP joint Refer to an orthopedic or hand surgeon

Asymmetric knuckle profile Metacarpal fracture X-ray, refer if fracture is present

Degenerative joint
disease

Finger “locks” or jumps with Trigger finger Refer to an orthopedic or hand surgeon
flexion

P r a c t i c e Pe a r l s f o r W r i s t a n d H a n d Pa i n

• Refer all patients with fractures early to an orthopedic surgeon or to ED if same-day ortho
follow-up is not accessible.
• If pain persists despite immobilization for 3 weeks, repeat x-rays to check for carpal fracture
or osteonecrosis, which may not be evident on initial films.
• Localization of pain

• Radial side: consider trauma, de Quervain’s tenosynovitis, or arthritis

• Ulnar side: consider cartilage tear (with trauma) or tendinitis
• Palmar side: consider CTS, ganglion cyst, or tenosynovitis
• For CTS, nonpharmacologic strategies that can help

• Have the patient hold the elbow next to the body and using the other
hand, forcefully extend the wrist for 10 seconds, 10 times tid-qid; this
stretches the carpal tunnel.
• Wear a wrist splint at night.
• Vitamin B6 100 mg bid may help with paresthesia; use NSAIDs prn for
pain.

503
Hip and low back pain

I. History: in addition to the usual questions, ask every patient about the following signs and
symptoms, which are red flags warranting immediate referral:

A. Bowel or bladder incontinence: consider lower disc disease or cauda

equina syndrome
B. Numbness in the “saddle area”: consider cauda equina syndrome
C. Pain suggestive of dissecting aortic aneurysm (severe “tearing” pain)
or cancer (back pain, especially if worse while supine, and history of
cancer)
D. Fever and/or weight loss (particularly in a patient with
immunosuppression, DM, or history of substance abuse or recent
spinal surgery)
E. In a patient aged <20 years or >55 years with no prior history of back
pain: consider ankylosing spondylosis, osteoporosis, infection, or
tumor
F. Unrelenting night pain (or no relief with bed rest) and/or difficulty in
finding a comfortable position
G. Risk factors for spinal infection
1. Known infection elsewhere
2. IV drug use
3. Systemic signs and symptoms, including fever
4. Lab evidence, including elevated WBC count and ESR
II. Physical examination (inspection/palpation/neuromuscular)

A. Watch the patient walk (abnormal gait often indicates hip disease);
have the patient walk on heels (L5) and then on toes (S1); if the patient
is able to do this, cauda equina syndrome is ruled out
B. Patient standing
1. Look at thigh muscles for atrophy
2. Look at the patient’s back for deformities (e.g., kyphosis, scoliosis) or
lateral curves
3. Look for height difference in shoulders, iliac crests, and skin crease
below buttocks

504
4. Palpate for levelness of iliac crests (not level: probably pelvic tilt)
5. Check ROM forward, backward, and to both sides
a) forward flexion decreases pain in spinal stenosis and increases pain in
sciatica
b) look for flattening of the lumbar curve
6. Press for tenderness along the sacrum and lateral buttocks
C. Patient sitting
1. Look again for atrophy of thigh muscles
2. Palpate for point tenderness; may percuss the vertebrae for pain
3. Palpate paravertebral muscles for tightness or bulge
4. Have the patient flex the hip upward (i.e., raise thigh) as you resist by
pressing down on the distal thigh
5. Check DTRs
6. The examiner extends each knee individually until the leg is straight
(passive straight leg raise)
D. Patient supine
1. Look for differences in leg length (may indicate a somatic dysfunction
for which chiropractic or osteopathic manipulation may help)
2. Auscultate and palpate the abdomen (to check for bruits and
aneurysm)
3. Palpate for pain along the anterior-superior iliac crest, over the greater
trochanter, and over lateral fibular heads
4. Flex the patient’s knee and hip and check internal and external rotation
in relation to pain
5. Abduct and adduct the straight leg (testing hip ROM)
6. Have the patient bend each knee (individually) up to the chest and
pull firmly against the abdomen; the opposite thigh should remain on
the table, fully extended
7. Check motor, sensory, and circulatory status (e.g., flexion of the great
toe against resistance, sensation along dermatomes [see Figure 14-1 for
dermatomes], capillary refill)

505
 8. Passive SLR bilaterally with the foot dorsiflexed: note the degree of
elevation causing pain (15 degrees to 30 degrees in severe cases, 30
degrees to 60 degrees in milder cases) and any radiation of pain down
the leg; pain must extend below the knee to be a positive test
9. If suspecting piriformis syndrome: have the patient lie on the
unaffected side, with the hip and knee flexed to 90 degrees. The
examiner stabilizes the pelvis with one hand and presses the flexed
knee to the table; this often reproduces pain in the buttock and even
down the leg.
III. Hip and low back pain diagnosis (see Tables 14-8, 14-9, & 14-10)

Table 14-8
Common Hip Disorders

Finding Possible Cause(s) Additional Points

Unequal leg length Fracture or dislocation Internal or external rotation also seen
Refer after examination

Limited ROM Arthritis With arthritis, internal rotation is lost early

Fracture
Dislocation

Active hip and knee flexion of one leg Flexion deformity of Consult an orthopedic surgeon or physiatrist
results in passive flexion of the other leg the passive hip

Pain radiates to the lateral knee Iliotibial band Often found in joggers
syndrome Treat with NSAIDs and hip adduction stretching
exercises

Tender to palpation along the lateral Trochanteric bursitis Treat with NSAIDs and stretches; possibly steroid
knee/greater trochanter injections

Limited ROM and progressive limp Aseptic necrosis Usually associated with a dull ache or throbbing
(osteonecrosis) of the pain in the groin, lateral hip, or buttock area
hip

Table 14-9
Common Low Back Pain Examination Findings

Muscle
Finding Possible Nerve Compression
Spasm
“Radicular” pain X
Pain radiates below knees X
Asymmetry on inspection or palpation X
Limited ROM X X
Paravertebral muscle bulge X
Positive SLR X (usually at 40 degrees-60 Possible
degrees)

506
 Asymmetric DTRs X
Asymmetric motor or sensory findings X
Unequal sacroiliac joints, sacral spines, or leg X
lengths

Table 14-10
Comparison of Lumbar Nerve Roots

Finding L4 L5 S1
Pain Lateral hip and Mid buttock to lateral buttock, Mid buttock, posterior leg,
anterior leg lateral leg lateral foot

Numbness Distal anterior thigh Lateral calf Posterior calf and lateral foot
and knee

Motor weakness Quadriceps extension Dorsiflexion of the great toe Plantar flexion of the foot

Reflexes Diminished patellar — Diminished Achilles tendon

reflex reflex

Screening examination (unable Squat and stand Walk on heels Walk on toes
to perform)

P r a c t i c e Pe a r l s f o r H i p a n d L o we r B a c k Pa i n

• A patient with an acute herniated disc prefers to stand.

• Disc disease and myofascial pain are most common in adults aged <50 years.
• Spinal stenosis, cancer, and Paget’s disease usually occur in adults aged >50 years.
• Spinal stenosis also involves numbness and/or weakness in legs with standing; improves or
resolves with sitting or bending forward.
• Bilateral hip pain that starts with walking and is relieved with rest: consider vascular or
neurogenic claudication.
• Plain x-rays showing osteoarthritis do not necessarily rule out other causes of hip pain.
• A phrase to help remember which type of CA metastasizes to the bone: “BLT with Mayo and
a Kosher Pickle” (Breast, Lung/lymphoma, Thyroid, Multiple myeloma, Kidney, Prostate).
• Young adolescent with hip or knee pain but no physical findings (except maybe a limp):
suspect slipped capital femoral epiphysis until ruled out with x-rays (AP and frog-legged
view); if present: emergent orthopedic referral.
• Referred pain to the hip may be from the following:

• Testicular torsion
• Lumbar spinal problem

507
 • Disorder of the pelvic cavity
• Vascular or neurogenic claudication
• Refer all patients with positive neurological findings for consultation and further diagnostic
studies; often, specialists may want MRI of the area done before patient’s appointment.
• Treatment for mechanical low back pain

• Advise the patient to avoid bed rest (including sitting in bed) and to
simply limit activities that increase pain. Improvement occurs in most
cases within a few weeks; mild symptoms may persist or recur.
• Encourage cold packs; the patient may alternate cold and hot packs.
• NSAIDs are given for pain; opiates may be needed short term to enable
the patient to begin exercise.
• Exercise is the key to treatment (e.g., walking, swimming, cycling).
■ Start as soon as possible, starting with 5 to 10 minutes and working up
to 20 to 30 minutes qd.
■ Abdominal (core) and back strengthening exercises may help prevent
future problems (although not consistently proven in research).
• Instruct regarding lifting and carrying techniques.
• Recheck if not improved in 1 week.
• Additional therapeutic modalities for cervical, thoracic, and
lumbosacral strains
■ Spinal manipulation (e.g., osteopathic, chiropractic)
■ Myofascial release, deep massage
■ P.T. for commonly used modalities
■ Trigger point injections with saline, Marcaine, or Xylocaine

Knee

I. History

A. Pain related to mechanical use (e.g., brought on by walking, climbing,

bending)
1. Sharp, stabbing pain: consider mechanical problem
2. Dull, aching pain: probably degenerative and overuse problems

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 3. Localization of pain can significantly narrow possible diagnosis
a) worse with repetitive flexion-extension movement with weight
bearing (e.g., going up or down stairs or squatting and then standing):
stress on extensor mechanism
b) worse with pivoting: meniscus or patella
c) increases during the day: degenerative arthritis
d) decreases during the day: inflammatory conditions (e.g., arthritis,
tendinitis)
B. “Clicking”: common and does not imply disease; may be associated
with a torn meniscus, arthritis, or chondromalacia
C. Buckling (i.e., knee “gives away”)
1. True: the patient cannot bear weight; associated with anterior cruciate
tear, torn meniscus, patellar dislocation
2. Pseudo: transient; often a disorder of the extensor mechanism (e.g.,
patellofemoral disorder or weak quadriceps muscles, especially in
elderly or sedentary individuals) or injury of the lateral or medial
collateral ligament
D. “Locking” of knee
1. Acute: usually related to trauma
2. Recurrent: usually due to a torn meniscus but may be degenerative
arthritis
E. Swelling
1. What area of the knee? Is it associated with redness and/or increased
warmth?
2. Constant or recurrent (what seems to cause it)?
II. Inspection

A. With the patient undressed below the waist, compare both knees
during the examination (Figure 14-7)
B. Watch the patient walk; evaluate symmetry of gait
C. Patient in the supine position with legs extended and relaxed, look for
the following:

509
 1. Atrophy of quadriceps muscles
2. Effusion (loss of normal knee hollow on the sides of the patella)
III. Palpation: examine the uninjured knee first; with the legs extended and relaxed, evaluate:

A. For thickening or swelling above and on the sides of the patella; to

identify a large effusion, perform ballottement
1. Firmly grasp the thigh just above the patella (forces fluid into the space
between the patella and femur); using two fingers of the other hand,
push the patella sharply back against the femur
2. Positive (abnormal) result is a palpable click
B. Patellofemoral compartment
1. Move the patella side to side
2. Push the patella distally and ask the patient to tighten the knee against
the table (contracts quadriceps muscles); note pain (“patellar grind”)
or crepitus (crepitus alone has little significance)
IV. ROM

A. Incomplete extension is the most subtle limitation

B. Limited ROM may be due to joint effusion, pain, or a mechanical
problem of the joint, menisci, or ligaments
C. Test the integrity of the collateral ligaments
1. Medial: with the leg extended, exert pressure on the lateral side of the
knee and medial side of the ankle
2. Lateral: with the leg extended, exert pressure on the medial side of the
knee and lateral side of the ankle
3. Positive (abnormal) result is pain and “opening up” of the knee
toward the side being tested
D. Perform McMurray’s test
1. Flex the knee while holding the heel of the foot in your hand, with the
ball of the foot resting on your wrist
2. Place your other hand on the joint line of the knee
3. Rotate the foot laterally and extend the leg: checks the medial
meniscus; rotate the foot medially and extend the leg: checks the
lateral meniscus

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 4. Positive (abnormal) result is a palpable, painful click
E. Tibiofemoral joint: flex the knee to 90 degrees with the foot on the
examination table
1. With your thumbs, press into the joint space on either side of the
patellotibial tendon and let your fingers surround the sides of the leg
(resting on top of the collateral ligaments and menisci); palpate for
tenderness or irregular bony ridges along the joint space
2. Palpate the extensor mechanism for tenderness: quadriceps tendon on
the superior patella and patellotibial tendon on the inferior patella
3. Palpate the medial and lateral areas of the knee for tenderness
4. Palpate the posterior surface of the knee for hamstring muscles (knee
flexors)
5. In an adolescent with knee pain, press on the tibial tuberosity and note
swelling or tenderness
F. Test the integrity of the cruciate ligaments (drawer tests)
1. Knee flexed with the foot flat on the table; sit on the foot and grasp
both sides of the tibia at the knee
2. Pull the tibia forward: tests the anterior cruciate ligament
3. Push the tibia back: tests the posterior cruciate ligament
4. Positive (abnormal) result is movement of the tibia away from the joint
V. Common knee disorders: see Table 14-11

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 FIGURE 14-7 Right Knee. Source: (From Rutter P, Newby D: Community Pharmacy:
Symptoms, Diagnosis, and Treatment, ed 2, Hamilton, Australia, 2008, Elsevier.)

Table 14-11
Common Knee Disorders

Possible
Finding Additional Points
Cause(s)
Loss of knee “hollows” Effusion Warm and tender: may be synovitis
Synovial Nontender: OA
thickening Positive bulge sign or fluid wave with effusion

Positive patellar ballottement Large effusion See above

Consult or refer to an orthopedic surgeon

Crepitus or pain with quadriceps tightening
Osteoarthritis PFS is the most common knee problem: treat with
Patellofemoral NSAIDs and decreased knee stress until improvement
syndrome is seen with VMO exercises (see Practice Pearls for
(PFS) Knee Pain)
Refer to P.T. if no improvement after 3-4 weeks

Pain and abnormal movement when testing Tear of the Refer to an orthopedic surgeon
collateral ligaments medial or

512
 lateral
collateral
ligament

McMurray’s test: positive results Torn meniscus Refer to an orthopedic surgeon

Pain with palpation of the tibiofemoral joint Damaged Positive results from McMurray’s test or weakness of
menisci or the medial or lateral collateral ligament
collateral Pain more over the tibial tubercle
ligament(s)
Bursitis

Bony ridges along the tibiofemoral joint Osteoarthritis

Swelling or pain over the tibial tuberosity Osgood- Normal quadriceps strength and ROM of knee
Schlatter
disease

Positive result from drawer tests Cruciate Refer to an orthopedic surgeon

ligament tear

Posterior knee pain Hamstring Refer to P.T.

strain or Refer to an orthopedic surgeon
tendinitis
Venous Doppler
Bakers cyst
DVT

Pain over the lateral femoral epicondyle ITB syndrome Refer to P.T.; NSAIDs routinely for 7-10 days

Severe pain in the extremity out of proportion Possible acute Emergent referral to ED
to what would be expected; sensation of compartment
tightness and swelling; worsened by passive syndrome
stretching

P r a c t i c e Pe a r l s f o r K n e e Pa i n

• With knee problems, also examine the hip, spine, and back because referred knee pain may
be from the following:

• Adults: herniated disc, muscle strain, hip injury

• Children: hip pathology
• MRI is rarely needed as part of the initial evaluation of knee complaints.
• Patella fractures may result from injuries such as falls; fracture of tibia or femur is usually
due to major trauma.
• With vastus medialis oblique (VMO) exercises, it takes 3 to 6 weeks to start seeing results. To
perform, have the patient sit with the legs extended either on the floor or sitting in a chair
with legs supported on another chair or footstool; fully dorsiflex the foot, press the knee

513
 down (i.e., against the floor), and hold for 10 seconds; do this 10 times bid.
• If the condition does not respond to nonsurgical therapies, refer to an orthopedic surgeon.

Foot and ankle

I. The foot is not often a site of referred pain; most significant structures are either palpable or
easily tested during physical examination; try to localize the problem to the forefoot, midfoot, or
hindfoot (Figures 14-8 & 14-9)
II. Inspection and palpation

A. Beginning away from the area of maximal pain, inspect and palpate
all surfaces for swelling (unilateral [i.e., localized] or bilateral [i.e.,
systemic]), deformities or nodules, calluses or corns, or point
tenderness
1. Ankle joint: over the anterior aspect, lateral and medial malleoli, and
ligaments
2. Achilles tendon
3. MTP joints
a) by “squeezing” the forefoot with your thumb and fingers just
proximal to the distal ends of the first and fifth metatarsals
b) palpate the distal end of each metatarsal individually using your
thumb and index finger
4. Plantar surface: for plantar warts, ulceration, tenderness on pressure
over the heel or ball of the foot
B. While you observe the patient from behind, have the patient stand on
toes barefooted; verify that both heels rotate inward (unequal with
posterior tibial tendon problem; refer to an orthopedic surgeon if
present)
C. With ankle injuries, squeeze the sides of the lower leg just distal to the
knee (tibia-fibula “squeeze test”)
III. ROM: perform actively or passively or both

A. Dorsiflexion (point the foot toward the patient)

B. Plantar flexion (point the foot away from the patient)
C. Inversion (twist the sole of the foot inward)
D. Eversion (twist the sole of the foot outward)

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 E. Flexion of toes
IV. Common foot and ankle disorders: see Table 14-12

FIGURE 14-8 Areas of Foot. Source: (From Benzon HT, Rathmell JP, Wu CL, Turk DC,
Argoff CE: Raj’s Practical Management of Pain, ed 4, Philadelphia, 2008, Elsevier.)

515
 FIGURE 14-9 Medial and Lateral Ligaments. Source: (From Fritz S, Grosenbach J:
Mosby’s Essential Sciences for Therapeutic Massage, ed 3, Philadelphia, 2008, Elsevier.)

Table 14-12
Common Foot and Ankle Disorders

Finding Possible Cause(s) Additional Points

Heel pain Plantar fasciitis Treat with rest, NSAIDs, heel
Bone spur pad, or orthotics

Tendinitis Local steroid injection may

help

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 Roll arch of the foot over a
frozen juice can
Refer if no improvement (it
often takes 6-12 mos for
symptoms to resolve)

Pain with palpation Sprain or fracture Consider consultation

Ankle pain with tibia-fibula “squeeze test” Fracture Refer to an orthopedic

surgeon

Unable to bear weight immediately after an accident Severe sprain or fracture Urgent referral to an
orthopedic surgeon

Unable to plantar flex foot or walk on toes; with the patient Rupture of Achilles tendon Urgent referral to an
prone, squeeze the calf muscle and the foot will point if the (if the foot does not move orthopedic surgeon
tendon is intact as described)

Unable to dorsiflex foot Injury to the tibiotalar joint Refer to an orthopedic

surgeon

Pain at the base of toes increases with squeezing the Morton’s neuroma Shoes with good support or
forefoot while pressing upward on the sole between the extra padding
third and fourth metatarsal heads NSAIDs
Refer to an orthopedic
surgeon or podiatrist if no
improvement

P r a c t i c e Pe a r l s f o r F o o t Pa i n

• To distinguish warts from calluses: warts have interruption of skin lines, blood vessels in the
core, and tenderness with squeezing the sides of the lesion.
• Medical conditions that may affect the feet include DM, PVD, neuropathy, inflammatory
arthritis, or gout.
• With bilateral foot pain, consider a systemic or spinal cause.
• Forefoot problems in women are often caused by high-heeled and/or ill-fitting shoes. Initial
treatment always includes shoe modification (i.e., low heels, wider or longer shoes).
• Plantar fasciitis is the most common cause of heel pain. If treatment modalities (see Table 14-
12) do not help, consider x-ray of the foot and referral to a podiatrist or orthopedic surgeon.
• The following findings suggest severe ankle injury, and the patient should be referred soon
to an orthopedic surgeon:

• Eversion injury (more serious: medial support is stronger)

• Immediate diffuse swelling (often indicates bleeding)
• Unable to bear weight immediately

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 • Tender “squeeze test” of the tibia and fibula
• Positive drawer test
• X-ray examination shows avulsion fracture or fracture of the foot

Strains and sprains

I. Strain: excessive stretch or tear of the muscle fibers

A. Common sports injury seen in activities such as jumping, running,

and kicking
B. A complete tear of a muscle is called a rupture
II. Sprain: excessive stretch of the ligament with disruption of its fibers

A. Commonly occurs in the knee, ankle, or wrist during physical activity

B. Uncommon in children with open growth plates or in a patient with
significant OP (bone injury or fracture more likely to occur in these
cases)
C. See Table 14-13 for clinical findings and treatment of sprains
Table 14-13
Comparison of Sprains

Grade
of Clinical Findings Suggested Treatment
Sprain
I Mild stretching of the ligament Symptomatic treatment only:
Pain and tenderness with little or no RICE*
swelling; no joint instability
NSAIDs round-the-clock, not prn, for 48 h
Able to bear weight with minimal pain When pain is resolved, begin active or passive ROM 3-4 times qid

II Significant but incomplete tearing of the Immobilization: posterior splint, air cast, or soft brace and non–
ligament weight-bearing with crutches until able to walk with normal gait
Moderate pain, swelling, and RICE*
ecchymosis with slight-to-moderate
NSAIDs round-the-clock, not prn, for 48 h
instability
When pain is resolved, begin ROM 3-4 times qid
“Pop” felt and often heard; defect
palpable May need opiates for pain

Weight bearing and walking are painful

III Complete ligament tear Refer to an orthopedic surgeon

Marked pain, swelling, tenderness, and Symptomatic treatment is controversial
ecchymosis with significant instability
Posterior splints and crutches
Unable to bear weight or walk NSAIDs round-the-clock for 48 h and opiates for prn use
*
RICE is an acronym for the treatment of many joint injuries:

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R Rest: avoidance of activities that cause pain; the length of time varies with the injury.
I Ice: 20 minutes qid, usually for 2 to 3 days; a convenient ice pack is a bag of frozen peas or corn, which can “mold” around an injury
and be refrozen as often as necessary (caution the patient to somehow mark the bag so that the vegetables are not accidentally eaten
after being thawed and refrozen).
C Compression: use of ACE bandage to provide support and limit swelling.
E Elevation: keep elevated as much as possible for 24 to 48 hours.

P r a c t i c e Pe a r l s f o r S t r a i n s a n d S p r a i n s

• With strains, try to gently stretch the injured muscle while palpating for a defect in the
muscle.
• If the patient is unable to contract the muscle to move a joint, consider complete rupture or
severe pain as the cause. Immobilize the joint and refer to an orthopedic surgeon.
• Order x-rays with suspected fracture, pain over malleoli or midfoot areas, or inability to bear
weight immediately after injury.

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General musculoskeletal disorders
Osteoporosis (OP)

I. Types

A. Primary: occurs in postmenopausal women (estrogen deficiency) or in

men and women aged >75 years (due to subtle, prolonged imbalance
between bone resorption and formation or reduction in vitamin D
synthesis)
B. Secondary: due to extrinsic factors such as chronic liver or kidney
disease, IBD, malabsorption, hyperparathyroidism, premature
menopause, or chronic PPI use
II. Signs and symptoms

A. Backache or pain, acute and chronic

B. Kyphosis or scoliosis, atraumatic fractures
C. Loss of height (>2 cm since last seen or >4 cm loss over lifetime)
D. No peripheral bone deformities
III. Risk factors for fracture(s)

A. Dietary
1. Inadequate calcium
2. Excessive phosphate
3. Inadequate vitamin D intake in elderly people
B. Physical
1. Immobilization or sedentary lifestyle
2. Previous fracture
3. Low body weight
4. Over 75 years of age
C. Social
1. Alcohol abuse, cigarettes
2. Caffeine >16 oz qd (e.g., coffee, tea, caffeinated soda, energy drinks)

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 D. Medical
1. Chronic diseases (e.g., liver or renal problems, ulcerative colitis,
history of Mason shunt)
2. Corticosteroids (e.g., patient with COPD, Addison’s disease)
3. Excess thyroid hormone replacement or hyperthyroidism
4. Males: androgen deprivation therapy for prostate cancer (e.g., Lupron)
5. RA
IV. Diagnostic tests

A. Bone mineral density (BMD) is the primary test; dual-energy x-ray

absorptiometry (DEXA) is the most thorough
1. Initially ordered in women aged >65 years or postmenopausal women
aged <65 years with clinical risk factors for fracture. Consider BMD for
men aged >70 years or sooner with loss of 1.5-inch height or with risk
factors for fracture.
2. Results (if not normal)
a) osteopenia: 1 to 2.5 standard deviations (SD) below the expected bone
mass
b) osteoporosis: >2.5 SD below the expected bone mass
B. X-ray of vertebrae not necessary unless vertebral fractures are
suspected
C. Consider labs with significant decline in BMD while on therapy: CBC,
ESR, possibly protein electrophoresis (to rule out multiple myeloma
and leukemia); TSH and free T4, serum calcium and possibly PTH, and
FBG (to rule out endocrine disease)
V. Treatment

A. Nonpharmacologic
1. Activity
a) maintain weight-bearing exercise (e.g., walking 45 minutes 4 times a
week); consider resistance training 2 times a week
b) avoid aerobic exercises (too much stress on bones)
c) consider physical therapy measures for back muscle spasm

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2. Diet
a) calcium intake of 1200 mg qd total (food and supplement)
(1) food sources (see Appendix A)
(2) calcium supplements 500 to 600 mg bid with meals
b) avoid excess phosphate (e.g., carbonated beverages)
c) encourage vitamin D 800 to 1200 IU qd
(1) sunlight for 15 minutes qd
(2) supplements (e.g., with calcium or in a multivitamin)
(3) food sources: seafood, eggs, organ meats, fish liver oils, vitamin D-
fortified dairy products
3. Smoking cessation (cigarette smoking accelerates bone loss)
4. Prevention of falls
B. Medications: prescribed for patients with OP or at high risk for
fracture/OP
1. Bisphosphonate therapy is first-line therapy: given first thing in the
morning with 8 oz of water only; nothing else orally for 30 minutes.
Caution: with poor dentition, have the patient see a dentist before
starting bisphosphonates.
a) alendronate (Fosamax) 10 mg qd or 70 mg qwk
b) risedronate (Actonel) 5 mg qd or 35 mg qwk or 150 mg qmo
c) ibandronate (Boniva) 150 mg PO qmo or 3 mg IV q3 mos
d) zoledronic acid (Reclast) 5 mg IV yearly
2. Raloxifene (Evista) 60 mg qd; if hot flashes occur, stop medication until
symptoms stop and then “wean up” (e.g., 1 day in week 1, 2 days in
week 2, 3 days in week 3, etc., until taking qd)
3. Teriparatide (Forteo) stimulates bone growth and is used mainly for
patients with a very high fracture risk or those who had fracture while
on bisphosphonate. Use for a maximum of 2 years, then restart
bisphosphonate to help maintain bone density.
4. Denosumab (Prolia) is used for patients with a very high fracture risk
or if intolerant to oral bisphosphonates; it is associated with increased

522
 infection risk
VI. Follow-up

A. Annual chemistry screening (as indicated), breast examination, and

mammography
B. Repeat BMD in 2 years after initiating therapy; if stable or improving,
repeat less frequently. If worsening, verify medication adherence and
repeat in 1 to 2 years.
C. Patient education
1. Fall prevention, balance
2. Body mechanics
3. Alert the patient taking bisphosphonates to report any vision loss or
eye pain
D. Bisphosphonates may be stopped after 5 years of use for most patients
(those with no previous vertebral fractures and for whom BMD is
stable); recheck BMD in 2 to 3 years

Common painful joint disorders

I. Rheumatoid arthritis (RA)

A. Description: symmetric, inflammatory polyarthritis of unknown

etiology; it affects at least three joints, including small joints of hands
and feet; does not affect DIP joints or thoracic/lumbar spine
B. Signs and symptoms
1. Joint stiffness on rising, lasting >1 hour; often improves with activity
2. Affected joints are red, swollen, and warm
3. Ulnar drift or deformities of fingers (swan neck, boutonniere) often
present
4. Malaise and/or fatigue often present
5. May have extraarticular manifestations but not early in the disease
(e.g., pleural effusion, HF, A-fib, anemia, vasculitis, neuropathy)
C. Diagnostic tests
1. Lab: RA factor (high sensitivity), ESR or CRP, ANA, CBC, CMP, UA;
consider anti-CCP (high specificity), serum uric acid, UA

523
 2. Consider x-rays of painful joints (e.g., hands)
D. Treatment
1. Refer to a rheumatologist
2. Monitor patients taking immunosuppressive agents for signs of HF
and skin cancers
3. No live vaccines (e.g., for shingles) if taking biologic DMARD agents
(e.g., Enbrel, Humira)
II. Osteoarthritis (OA)

A. Description: noninflammatory degenerative changes in joints related

to past trauma, aging, and/or obesity
1. Common in weight-bearing joints (e.g., hip, knee, spine) and DIP/PIP
joints and base of the thumb
2. Joints usually spared: wrist, elbow, ankle (unless previous fracture)
B. Signs and symptoms
1. Joint stiffness on rising, lasting <30 minutes; occurs more by the end of
the day
2. Affected joints are irregularly shaped but not red or warm; pain is dull,
achy, worse with activity, and improves or relieved with rest
3. May have nontender Heberden’s (DIP) and Bouchard’s (PIP) nodes
4. There are no extraarticular manifestations
C. Diagnostic tests: consider especially with knee or hip pain or
symmetrical pain in hands
1. Lab: ESR, RA factor
2. X-ray of the affected joint(s)
D. Treatment
1. Nonpharmacologic
a) weight loss, if indicated
b) rest joint 12 to 24 hours with acute pain, then resume ROM and
exercise (especially aquatic exercise)
c) consider physical therapy

524
 d) use of items such as cane, shoe orthotics
2. Pharmacologic
a) acetaminophen or NSAIDs (if acetaminophen is not effective)
b) tramadol with acetaminophen 37.5/325 mg 1 to 2 tabs qid prn
c) glucosamine sulfate 1500 mg qd (shellfish allergy is not a problem with
this)
d) consider intraarticular steroid injection or Hyalgan injections
3. With no response to therapy or functional limitations and pain at rest
or at night: refer to an orthopedic surgeon
III. Gout

A. Description: clinical syndrome resulting from urate crystals deposited

in the tissue, with inflammation and potential destruction of the tissue
or joint. All patients with gout will have hyperuricemia at some point,
but most people never experience a gout attack.
1. Primary hyperuricemia: no coexisting disease or drug that alters uric
acid production or excretion
2. Secondary hyperuricemia: excessive urate production or diminished
renal clearance (see risk factors below)
3. Can affect several different joints, but usually only one at a time; often
involves the big toe (MTP joint). Very rarely affects the spine.
B. Risk factors
1. Dehydration
2. Dietary: fatty food, increased intake of red meat and seafood/fish
3. Alcohol (men only): 2 drinks qd, beer or distilled spirits
4. Diuretic use
5. Comorbid conditions: HTN, DM, obesity or weight gain,
hyperlipidemia, trauma
C. Signs and symptoms
1. Acute stage: joint effusion—joint is red, warm, and very tender (“even
the sheets hurt”); reaches maximum inflammation within 24 hours.
There is no fever or leukocytosis.

525
2. Chronic gout: may have large, painless nodules (tophi), especially over
the MTP or MCP joint
3. May have kidney stone(s)
D. Diagnostic tests
1. Consider CBC, ESR (if unsure of diagnosis)
2. Serum uric acid: not recommended with acute attack; most accurate
time for baseline level or monitoring therapy is at least 2 weeks after
resolution of acute flare
3. Gold standard is seeing urate crystals in joint fluid aspirate (usually
done by a rheumatologist)
E. Treatment
1. Acute flare: most effective when started within 48 hours of symptoms;
consider comorbidities before choosing treatment
a) NSAIDs: indomethacin 50 mg tid or naproxen 500 mg bid; may taper
as symptoms improve but continue until pain-free, up to 1 week;
consider using PPI while taking NSAIDs
b) colchicine 0.6 mg tid first day, then 1 to 2 times qd until pain resolves
c) prednisone 30 to 50 mg in bid dose for 2 to 5 days, then taper over 7 to
10 days
2. Recurrent or chronic gout
a) after second or third attack, check uric acid levels and consider
prophylactic therapy, usually with allopurinol
(1) start with 100 mg qd (with normal renal function) and increase by 100
mg every few days; may take up to 800 mg qd. Start with 50 mg qd
with renal insufficiency and titrate more slowly.
(2) give colchicine 0.6 mg 1or 2 qd or NSAIDs qd for 6 months to prevent
gout flares
b) instead of allopurinol, may use febuxostat (Uloric) 40 to 80 mg qd
c) uric acid goal is <6 mg/dl
3. Refer to a rheumatologist if not responding to therapy
F. Address prevention when between gout attacks (most patients have
second attack within 2 years)

526
 1. Lifestyle changes and managing comorbid diseases
2. Instruct the patient to start NSAIDs when acute symptoms start,
without waiting to consult the provider each time

Fibromyalgia syndrome

I. Description

A. Fibromyalgia is a common cause of chronic musculoskeletal pain; the

etiology is unknown
B. There are no physical changes and it is not life threatening, but is
usually chronic and often disabling from a functional viewpoint. It is
often associated with the following:
1. Lack of stage 4 (deep) sleep
2. Increased incidence of OA, SLE, and RA
II. Diagnosis

A. Characterized by widespread aching above and below the waist and

both right and left sides of the body for at least 3 months plus
B. Multiple tender points (Figure 14-10) that often come and go
1. Check for tender points using the same amount of pressure used to
blanch the thumbnail; in clinical practice, a specific number of tender
points is not required to make diagnosis
2. Consider checking “control locations” (e.g., thumb, forehead), which
are usually not tender
C. Associated symptoms: the more that are present, the more secure the
diagnosis. Major associated symptoms are italicized.
1. Fatigue (especially when arising from sleep but also mid-afternoon)
2. Morning stiffness
3. Sleep disturbances (not insomnia, but not restful)
4. Paresthesias (often migratory and may last for several hours)
5. H/A (includes migraine and muscle tension headaches)
6. Anxiety and depression
7. Cognitive disturbances: “fibro fog,” including problems with attention

527
 and concentration
8. Subjective swelling
9. Irritable bowel syndrome
10. Breathlessness, palpitations
11. Dizziness
D. Fibromyalgia often worsens with the following:
1. Anxiety and stress
2. Temperature changes
3. Humidity and weather changes (barometric pressure)
4. Fatigue, poor sleep
E. Detailed history and examination are most helpful; x-rays, CT and
MRI scans, and EMG studies are unnecessary unless some other
diagnosis is suspected
F. Diagnostic studies are of little benefit except to rule out other causes
1. Hypothyroidism (TSH, free T4)
2. Muscle disease or polymyalgia rheumatica (ESR or CRP, liver
enzymes)
3. Chronic infection (CBC)
4. Sleep apnea and RLS (overnight sleep study)
III. Treatment

A. A multidisciplinary team works best: PCP, psychologic or psychiatric

support, physical therapist, occupational therapist, massage therapist,
and rheumatologist
B. Because there is no known cure, an individualized, holistic treatment
plan offers the best chance for management and improvement of
symptoms
C. Nonpharmacologic care (some patients respond to these without
needing medication)
1. Education: diagnosis and treatment of fibromyalgia, uncertainty of the
cause, and patients’ role in their own treatment
2. Gentle, low-impact aerobic exercise tailored to meet specific needs;

528
 suggestions include walking slowly and consistently (e.g., 5 minutes)
on alternate weekdays and increasing 5 minutes q2 weeks with a goal
of 20 to 30 minutes 3 to 5 times qweek by the end of the first year, or
water therapy
3. Physical therapy modalities (e.g., heat and gentle massage)
4. Biofeedback, hypnosis, and acupuncture may be of benefit
5. Smoking cessation
6. Adequate sleep and nutrition; consider sleep studies if sleep apnea is
suspected
D. Pharmacologic therapy (symptomatic; no treatments are curative)
1. NSAIDs, opiates, and corticosteroids are ineffective
2. Amitriptyline (Elavil) 10 mg hs; may increase by 5 mg q2 weeks till
maximum relief of symptoms is achieved without unacceptable side
effects (usually 35 to 50 mg qd)
3. Cyclobenzaprine (Flexeril) 5 to 10 mg hs
4. Tramadol or tramadol with acetaminophen (Ultracet) 1 to 2 tabs q4-6h,
up to 8 tabs in a 24-hour period can help pain (try amitriptyline or
cyclobenzaprine first)
5. If not responding to amitriptyline or having intolerable side effects, try
duloxetine (Cymbalta) 20 to 60 mg qd or pregabalin (Lyrica) 25 to 50
mg hs, increasing up to 300 to 450 mg qd or milnaciprin (Savella) 12.5
to 100 mg bid
6. Gabapentin (Neurontin) 100 to 300 mg hs for peripheral pain

529
 FIGURE 14-10 Tender Points for Fibromyalgia Syndrome. Source: (From Lewis
SL, Dirksen SR, Heitkemper MM, Bucher L: Clinical Companion to Medical-Surgical Nursing,
ed 8, St. Louis, 2011, Elsevier.)

P r a c t i c e Pe a r l s f o r F i b r o m ya l g i a

• Inform the patient that there is no cure, but teamwork between the patient and providers
can be beneficial.
• If “resistance” develops to amitriptyline or cyclobenzaprine, stop the medicines for 4 weeks
and avoid all medicines that inhibit serotonin uptake receptors; consider the following:

• Alprazolam 0.5 to 1 mg or clonazepam 1 mg hs

• Carisoprodol 350 mg hs (patient can also take 1 to 2 tabs tid)
• If inadequate response to therapy, refer to a specialist (e.g., rheumatologist, physiatrist,
psychiatrist, pain management).
• Encourage the patient to prioritize time and activities (e.g., work, leisure, ADLs).

Restless leg syndrome (RLS)

530
I. Description: RLS is a syndrome characterized by unpleasant sensations in the legs that occur at
rest and are relieved by movement

A. Although long remissions are possible, the condition is generally

chronic or recurrent
B. RLS often occurs in association with DM, end-stage renal disease, and
pregnancy
C. With positive FH of RLS (>40% cases), symptoms are more likely to
begin when <45 years of age and are often associated with iron-
deficiency anemia.
D. May be triggered by smoking, fatigue, sleep deprivation, or by
stopping or starting certain medications. These medications include
the following:
1. Antidepressants: amitriptyline, fluoxetine, paroxetine, mirtazapine
2. Antihistamines: fexofenadine, loratidine, diphenhydramine
3. Lithium
4. CCB: verapamil (Calan), diltiazem (Cardizem), amlodipine, nifedipine
(Procardia)
5. Major tranquilizers: haloperidol, quetiapine, thorazine
II. Diagnostic criteria

A. The almost irresistible desire to move legs usually associated with

paresthesias (e.g., sensations described as creepy, crawling. or
drawing)
B. Symptoms are worse or present only at rest and are at least partially or
temporarily relieved during activity. They are worse in the evening or
at night.
III. Additional findings that may be present

A. Sleep disturbances (e.g., difficulty falling and remaining asleep,

exhaustion)
B. Involuntary movements (e.g., periodic jerking)
C. Normal neurological examination
IV. Treatment

A. Check serum iron and ferritin levels and if low, give iron supplement
(e.g., ferrous sulfate 325 mg) with vitamin C 100 to 200 mg bid to get

531
 ferritin levels to >50 mcg/L
B. Nonpharmacologic remedies may help
1. Hot baths or heat or ice pack to legs
2. Leg massage
3. Regular exercise
4. Avoiding aggravating factors (i.e., sleep deprivation, caffeine, nicotine,
ETOH)
C. Pharmacologic therapy
1. Dopamine agonist is the first-line treatment; take ∼2 hours before RLS
symptoms start
a) ropinirole (Requip) 0.25 mg qd; may increase by 0.25 mg q2-3d until
symptoms are controlled
b) pramipexole (Mirapex) 0.125 mg qd; may increase by 0.125 mg q2-3d
until symptoms are controlled
2. If dopamine agonist is ineffective, opiate (e.g., hydrocodone 1 to 2 tabs
hs) or tramadol (with or without acetaminophen) may be used
3. Some patients respond to anticonvulsants or benzodiazepines
a) gabapentin 100 to 300 mg bid or gabapentin enacarbil (extended
release) 600 mg early evening or
b) pregabalin 150 to 300 mg in the evening or
c) clonazepam 0.5 to 1 mg in the evening (unlabeled use)
4. Cyclobenzaprine 10 mg hs may help
V. Refer to a sleep specialist or neurologist if therapy is not as effective as the patient would like

532
CHAPTER 15

533
Pain
Assessment of pain

I. A common method for identifying pain is to use a rating scale (e.g., 0 to 10, with 0 being no
pain and 10 being the worst pain imaginable) II. Consider the following when a patient cannot
communicate in a meaningful way:

A. Attempt to obtain a self-report

B. Ascertain how the patient usually exhibits pain (i.e., from family, past
clinicians)
1. Patients with dementia or other disabilities may or may not be able to
accurately report pain and may exhibit confusion, irritability, loss of
appetite, or frequent falls 2. Children may have aggressive outbursts,
become withdrawn, eat excessively, or have a poor appetite
III. History related to pain

A. Does the patient take any pain medications regularly? If so, how often
and for what kind of pain? Are they effective?
B. With chronic pain, what is the impact on the following:
1. Overall quality of life and functioning (e.g., socializing, relationships,
mood and anxiety, sleep, exercise, and occupation) 2. Basic ADLs and
activities required to live independently (e.g., shopping, preparing
meals, doing housework, managing finances and medications)
IV. PMH related to pain

A. Ask about prior evaluations and treatment of pain

B. Current and past providers (including alternative practitioners) and
reasons for visits C. Past medications prescribed and effects
D. Any tests/imaging studies done in the past 10 years
E. Was pain associated with trauma, surgery, or illness?
F. Is there any litigation pending?

Acute pain

534
I. Description

A. Usually lasts up to 3 to 6 months and is treated with appropriate pain

medication, PT, or home care B. Expected to be self-limiting
C. Can be caused by trauma, surgery, or illness
II. Treatment: includes medications (e.g., NSAIDs, tramadol, opiates); may also include
nonpharmacologic therapies (see Therapies for Pain, later in this chapter)

Chronic pain

I. Description

A. Pain persisting longer than 6 months

B. May be continuous, intermittent, or a combination of both C. Often
associated with sleep or appetite disturbances, irritability, social
withdrawal, depression D. Often, there is a disparity between
examination and/or diagnostic tests and the level of patient complaints
(e.g., patient rates pain as a 10 and no pain is elicited on examination)
II. Types of chronic pain

A. Neuropathic pain (onset may be weeks to months after acute nerve

injury)
1. Peripheral pain
a) caused by PHN, DM neuropathy, and nerve damage
b) described as “pins and needles,” “on fire,” aching, crushing,
paroxysmal stabbing, “electric shocks”
c) may respond better to anticonvulsant or antidepressant medications
(see Therapies for Pain, Pharmacologic Therapies, following this
section); poor response to opiates d) certain medications are used to
treat specific conditions (e.g., carbamazepine for trigeminal neuralgia)
e) with PHN, lidocaine 5% gel or patch can be effective
2. Central pain
a) caused by post-CVA, MS, and phantom pain
b) described as a loss of sensation with brief bursts of sharp pain, steady
burning sensation, allodynia (i.e., pain due to a stimulus not normally
painful, such as temperature or physical stimuli) c) may respond better
to tricyclic antidepressants, pregabalin, gabapentin; lidocaine 5% patch

535
 or gel has also been shown to be effective d) there may be a more
positive response to opiates in some cases; but antidepressants and
anticonvulsants should be tried first e) TENS unit therapy may work
well
B. Musculoskeletal pain
1. Acute pain usually associated with physical injury or overuse
a) well localized, aching, throbbing
b) may be intermittent or constant
c) treatment: conservative therapy with RICE and NSAIDs,
acetaminophen, and nonopiate pain meds (e.g., lidocaine 5% gel or
patch)
2. Chronic pain usually associated with degenerative joint disease and/or
chronic overuse
a) more continuous, achy, and dull; does not resolve but the patient may
manage with medications and lifestyle changes b) examples are back
pain, myofascial pain syndrome, OA
c) acetaminophen or NSAIDs can help; opiates should be used
chronically only in patients assessed to have a low risk of substance
abuse and who have pain despite trying other nonopiate pain meds
and antidepressants d) behavioral modification, PT, acupuncture, or
massage may benefit
3. Inflammatory pain is associated with chronic inflammation in joints or
infection that destroys the musculoskeletal surface areas
a) pain is caused by innocuous stimuli without trigger; there may be
obvious deformity or swelling of the area b) described as a sharp or
dull pain in the deformed-appearing joint c) examples are rheumatoid
arthritis, gout, psoriatic arthritis d) treatment includes NSAIDs,
DMARDs, and nonpharmacologic therapies such as light exercise,
heat, and OT/PT
C. Visceral pain
1. Is diffuse, poorly localized, and noxious
2. May be dull, aching, deep, cramping, and squeezing
3. Examples are renal calculi or any type of damage to internal organs 4.

536
Treatment is alleviation of the underlying cause of pain and may
require opiates, antispasmotics, benzodiazepines, and NSAIDs

537
Therapies for pain
Nonpharmacologic therapies

I. Often helpful in giving patients some control over their pain (acute and chronic); combination
therapies have been shown to be more effective than any single approach for managing chronic
pain II. Environmental

A. Comfortable lighting and temperature

B. Positioning with pillows, blankets, etc.
III. Distraction techniques (e.g., music, puzzles, or games) IV. Relaxation techniques
V. Educational programs pertinent to diagnosis
VI. Self-hypnosis, psychotherapy, or cognitive behavioral therapy VII. Physical modalities

A. Chiropractic
B. Massage, therapeutic touch
C. Physical therapy (including TENS, heat therapy)
D. Acupuncture
E. Exercise programs
VIII. Herbal products (not exclusive)

A. Comfrey topical preparation for bruises, pulled muscles, or sprains;

do not use on broken skin, for >6 weeks, or if pregnant B. Aloe topical
gel or spray for burns
C. Witch hazel topically to treat skin inflammation; not intended for use
PO

Pharmacologic therapies

I. NSAIDs

A. Antiinflammatory and analgesic properties (most effective with

inflammatory conditions) B. If one NSAID is not effective or tolerated,
consider trying a different one
C. Cautions
1. GI toxicity (e.g., gastritis, GI bleeding, ulcers); consider PPI to decrease
GI risk 2. May significantly affect renal function, especially with

538
 comorbid HTN or in elderly patients 3. All prescription NSAIDs have
a Black Box warning regarding CV effects; serious skin reactions are
also possible (e.g., Stevens-Johnson syndrome, toxic epidermal
necrolysis [TEN]) 4. Consider periodic liver and renal function tests
and CBC if using long term
II. Acetaminophen

A. Analgesic, antipyretic (no antiinflammatory properties) B. In

combination prescription medications, the individual dose is limited to
325 mg C. Cautions
1. Hepatic toxicity (consider periodic liver function testing) 2. Be aware
of other OTC medications that the patient is taking; many may contain
acetaminophen (maximum dose is 3000 mg qd) 3. Possible serious skin
reactions (e.g., Stevens-Johnson syndrome, TEN)
III. Muscle relaxers

A. Uses
1. Muscle spasms: associated with current or prior injuries (e.g., bursitis,
herniated disc, excessive stretching) 2. Spasticity: muscle fibers do not
relax well; often associated with a permanent condition (e.g., head
injury, CP, CVA, spinal cord injury)
B. Types
1. Centrally acting
a) relieve symptoms of spasm
b) include cyclobenzaprine, orphenadrine, carisoprodol, metaxalone,
methocarbamol
(1) may cause sedation; use cautiously with weakness, ataxia,
lightheadedness (2) carisoprodol has addictive concerns and is a
controlled substance in some states
2. Peripherally acting
a) used for spasticity
b) include baclofen, botox, tizanidine
c) may cause sedation, confusion, increased weakness, nausea, dry
mouth
C. Cautions

539
 1. Monitor for weakness and gait disturbance in elderly patients taking
muscle relaxers 2. Consider periodic liver and renal function tests if
using long term
IV. Opiates

A. Used to relieve moderate-to-severe pain (e.g., acute or chronic

[cancer]). They should be used chronically only in patients assessed to
have a low risk of substance abuse and who have pain despite trying
other nonopiate pain meds and antidepressants.
B. Types
1. Opiates (i.e., narcotic) with or without acetaminophen 2. Nonopiates:
tramadol (not fully related to opiates but binds to the same receptor)
with or without acetaminophen
C. Cautions
1. May cause drowsiness, oversedation, confusion, hallucinations,
decreased ability to make accurate judgments 2. When prescribing
opiates, initiate a prophylactic bowel regimen to prevent constipation
(see Chapter 10, Practice Pearls for Bowel Conditions) 3. Use
cautiously with COPD or other acute/chronic respiratory illnesses
because of possible respiratory depression 4. Avoid concurrent use of
CNS depressants and ETOH. SSRIs (especially paroxetine and
fluoxetine) and duloxetine significantly decrease the efficacy of
opiates.
V. Adjuvant therapies: for enhancing analgesics and managing other symptoms associated with
chronic pain

A. Antidepressants
1. SNRIs (e.g., duloxetine for neuropathy, fibromyalgia, chronic low back
pain) 2. Tricyclics (e.g., amitriptyline, nortriptyline, or desipramine)
B. Anticonvulsants for neuropathic pain
1. Gabapentin: usually tid dosing for PHN, painful DM neuropathy 2.
Pregabalin: usually bid dosing for PHN, DM neuropathy, fibromyalgia
3. Carbamazepine: bid dosing for trigeminal neuralgia
C. Topical preparations
1. Lidocaine 5%: patch, apply up to 3 patches in a single application and
may leave in place for up to 12 hours in any 24-hour period; gel, apply

540
 up to qid to the area of pain, maximum of 300 mg/24-hour period 2.
Capsaicin (e.g., Zostrix OTC cream): while wearing gloves, apply to
the affected areas at least tid-qid (less often decreases efficacy)
D. Injectable
1. Trigger point injections
2. Steroid joint injections
3. Epidural steroid injections
E. Oral steroids (e.g., prednisone, dexamethasone) for inflammatory pain
(dose individualized) F. Neurostimulator implants are options for back
pain
G. To help sleep: trazodone 25 to 150 mg hs, diphenhydramine 25 to 50
mg hs, amitriptyline 25 to 50 mg hs H. May need anxiolytics to
decrease stress and anxiety (see Table 18-2) I. Evaluate testosterone
levels because of the potential for impotence with chronic pain
medication J. Psychological counseling should be done routinely as
part of chronic pain care

P r a c t i c e Pe a r l s f o r T r e a t m e n t o f Pa i n

• When developing a treatment plan, consider the ultimate goal of therapy (e.g., comfort or
restoration of function).
• Use a stepwise approach for pain medications (see Table 15-1 for suggested therapies).
Table 15-1
Suggested Therapies for Pain

Pain Level Neuropathic Pain Nonneuropathic Pain

Mild-to-moderate pain Adjuvant therapy Nonopiate analgesic
(1-4 out of 10) +/− nonopiate analgesic +/− adjuvant therapy
Moderate pain Adjuvant therapy Weak opiate analgesic*
(4-7 out of 10) +/− weak opiate analgesic* +/− adjuvant therapy
Severe pain Adjuvant therapy Strong opiate analgesic†
(7-10 out of 10) +/− strong opiate analgesic† +/− adjuvant therapy
*
Weak: acetaminophen with codeine or oxycodone or hydrocodone, butorphanol.
†Strong: morphine, oxycodone, fentanyl, hydromorphone.

• In patients with a history of substance abuse, short-acting opiates may cause craving for
drugs because of pain cycling during the day; long-acting opiates may control pain more

541
 consistently and decrease craving.
• Opiates should be reserved for patients with moderate-to-severe chronic pain that is
adversely affecting function or quality of life.

• Chronic pain is best treated via round-the-clock dosing with long-

acting medication and with short-acting medication for breakthrough
pain prn.
■ Titrate the long-acting medicine as necessary q24-48h for severe pain;
an easy way to determine a new dose is to add the total mg of the long-
and short-acting doses given in a 24-hour period; this becomes the new
long-acting dose for a 24-hour period.
■ For breakthrough pain, use the short-acting form of the medication
used for long-acting pain (i.e., if using MS Contin as the long-acting
med, use MS IR as the short-acting med).
■ The short-acting med can also be given preemptively before bath, PT,
and other events.
• See Table 15-2 for narcotic equianalgesic dosing chart (i.e., dose
comparable to morphine 10 mg IM).
Table 15-2
Narcotic Equianalgesic Dosing*

Drug Route Equianalgesic Dose (mg)

Morphine IM 10
PO 30
Oxymorphone (Opana) PO 10
Hydromorphone (Dilaudid) IM 2
PO 8
Oxycodone (OxyContin) PO 20-30
Hydrocodone (e.g., Lortab) PO 30-45
Codeine IM 100-130
PO 200
Butorphanol (Stadol) IM 3
Intranasal 1 spray (1 mg)
Fentanyl (Duragesic) IM 0.1
Transdermal 12 mcg/h
*Each dose listed is equal in analgesia to morphine 10 mg IM.

• Opiate contracts

• Initiate when prescribing chronic opiate therapy.

■ Specify ALL controlled substances and other potentially addictive
medications (i.e., tramadol, butalbital, carisoprodol).

542
■ Signed by the patient and provider.
■ Include an agreement to obtain opiates from only one provider and one
designated pharmacy.
■ The patient is responsible for the written prescription and medication
(i.e., if either is lost, they will not be replaced), and for obtaining refills
during regular office hours.
■ Include consequences if the agreement is not followed (i.e., no further
controlled substances will be prescribed).
• The patient agrees to random urine drug screens.
■ Used to verify appropriate use (i.e., the prescribed drug should be
present) and to see if any other drugs are being taken.
■ Shows substance(s) used in previous:
• 3 days: amphetamines, cocaine, opiates
• 7 days: marijuana (up to previous 1 month with moderate-to-heavy
use) • 14 days: phencyclidines (e.g., ketamine, dextromethorphan)
■ False-positive results secondary to drug interactions with specimen
solution may occur (Table 15-3); a positive screening test should be
confirmed with a more specific test (usually gas chromatography/mass
spectrometry [GC-MS]).
Table 15-3
Possible False-Positive Test

Substance/Medication Taken False-Positive Result

Vicks inhaler Amphetamine/meth
Pseudoephedrine Amphetamine
NSAIDs, marinol Barbiturate/cannabinoid
Fluoroquin (levofloxacin, ofloxacin), ranitidine Opiate
Sertraline Benzodiazepine
Venlafaxine Phencyclidine
Dextromethorphan Phencyclidine, opiate
Poppy seeds Morphine/codeine

■ False-negative results may occur if the wrong screening panel is used;

let the lab know what you are looking for so that they screen for the
appropriate drug.
■ Medications taken as a patch will not show up in a drug screen.

543
■ If the patient admits to past substance use/abuse, consider increased
frequency of random urine drug screens and before refills.
• Refer to a pain specialist if the symptoms are debilitating or do not respond to initial
therapies or for increasing need for pain medication.

544
CHAPTER 16

545
Endocrine conditions
Thyroid disorders

Goiter

I. Signs and symptoms

A. The thyroid may be multinodular

B. The thyroid may be very large and compress the trachea
C. Related to inadequate iodine in the diet
II. Diagnostic tests

A. TSH and free T4 may indicate overactive or underactive thyroid

function B. Thyroid ultrasound
C. Consider thyroid radioactive iodine scan (nuclear scan)
III. Treatment

A. Consider consultation with/referral to an endocrinologist

B. Iodine supplementation (goiter usually does not shrink with
treatment)

Hypothyroidism

I. Signs and symptoms

A. General
1. Weakness, fatigue, lethargy
2. Cold intolerance
3. Mild weight gain or difficulty losing weight
4. Depression; confusion (in elderly patients, this may be the only sign)
B. Integumentary
1. Dry skin and/or hair
2. Hair loss, including loss of the lateral third of eyebrows

546
 3. May have brittle nails
C. Cardiac: bradycardia, possible cardiac enlargement
D. Genitourinary: amenorrhea, menorrhagia, infertility
E. Gastrointestinal: constipation
F. Metabolic
1. Complains of feeling cold easily
2. Hypercholesterolemia
3. Elevated CK
4. Hyponatremia
5. Macrocytic anemia
G. Neurological: slow DTRs (e.g., patellar and ankle jerk), slow speech
II. Diagnostic tests: elevated TSH and low free T4

A. If the patient has signs and symptoms but normal lab results, consider
depression B. With elevated TSH but normal free T4, consider
subclinical hypothyroidism
1. With TSH ≥10 U/L: treat with levothyroxine to normalize TSH and
decrease the risk of progression to overt hypothyroidism 2. With TSH
4.5 to 10 U/L: routine treatment is controversial; consider
levothyroxine with symptoms suggesting hypothyroidism
III. Treatment

A. Levothyroxine is the medication of choice; start with 25 to 50 mcg qd

(25 mcg qd with heart disease or age >60 years) and increase by 25 mcg
qd q2 mos until TSH normalizes. Then recheck lab yearly and prn.
B. It is most effective when taken on an empty stomach with no other
meds; if unable to take on an empty stomach, be consistent with when
it is taken C. Some patients may be taking thyroid USP
1. Adjust doses by 15 mg qd
2. 60 mg thyroid USP = 100 mcg levothyroxine in potency
3. Thyroid USP metabolism may be erratic
D. Consider brand name Synthroid if unable to correct TSH with generic
levothyroxine

547
Hyperthyroidism

I. Signs and symptoms

A. Thyroid: firm, smooth, or nodular goiter

B. General
1. Hyperactivity, nervousness
2. Anxiety, fatigue
3. Weight loss (unintentional)
4. Increased perspiration
5. Heat intolerance
C. Eyes
1. Stare and lid lag
2. May have exophthalmos (with Graves’ disease)
D. Cardiac
1. Tachycardia or atrial fib; palpitations
2. Angina, HTN
E. Neurological
1. Fine tremor of hands, tongue, or closed eye lids
2. Hyperreflexia
3. Proximal muscle weakness
F. Genitourinary
1. Female: amenorrhea or oligomenorrhea
2. Male: gynecomastia and/or erectile dysfunction
II. Diagnostic tests

A. TSH very low

B. Increased free T4
III. Treatment

A. If lab results are abnormal, obtain thyroid radioactive iodine (nuclear)

scan and refer for further medical therapy or surgery; do not order a
scan if the patient is pregnant or breast-feeding B. Atenolol 50 to 100

548
 mg qd can help control symptoms (while waiting to see an
endocrinologist)
C. Management of hyperthyroidism should involve an endocrinologist

Thyroid cancer

I. Signs and symptoms

A. Enlarged thyroid or a painless, hard nodule

B. Palpable lymph nodes, dysphagia or hoarseness
II. Diagnostic findings

A. Normal thyroid function tests (TSH and free T4)

B. Thyroid nuclear scan
1. “Hot” nodule: evaluate for hyperthyroidism and consider referral to
an endocrinologist or surgeon 2. “Cold” nodule: obtain a diagnostic
thyroid U/S and if a nodule is present, refer for fine-needle aspiration.
A “cold” nodule is a more serious finding and would be more often
seen with thyroid cancer.
III. Treatment: refer to an endocrinologist or surgeon for biopsy

P r a c t i c e Pe a r l s f o r T h y r o i d C o n d i t i o n s

• Laboratory tests (Table 16-1)

• Serum thyroid-stimulating hormone (TSH) is the primary test; if TSH is

abnormal, repeat TSH along with free T4.
• Serum thyroxine (T4): many factors may alter serum T4 measurements,
including acute illness, high estrogen states and hormone replacement
therapy, acute psychiatric problems, kidney and liver disorders, and
certain drugs.
• If thyroid dysfunction is suspected, also check lipid panel, basic
metabolic profile, and CBC levels and obtain an ECG.
• If the patient has unexplainable urticaria, check for thyroid dysfunction.

549
 • Screen asymptomatic patients who may be at increased risk for hypothyroidism

• Presence of goiter
• History of autoimmune disease
• Previous radioactive iodine therapy
• Previous head or neck radiation
• Family history of thyroid disease
• Taking medications that may impair thyroid function (e.g., lithium,
amiodarone)
• Biopsy is preferable with thyroid nodules.
• With a thyroid nodule >1 cm (by palpation and/or imaging): perform history and
examination and obtain TSH; if TSH is low, obtain thyroid nuclear scan.

• “Hot” nodule: evaluate for hyperthyroidism and consider referral to an

endocrinologist or surgeon • “Cold” nodule: get diagnostic thyroid
ultrasound and if a nodule is present, refer for fine-needle aspiration.
A “cold” nodule is a more serious finding.
Table 16-1
Laboratory Findings in Thyroid Disorders

Condition Free T4 TSH

Primary hypothyroidism (thyroid disease) ↓ ↑
Secondary hypothyroidism (pituitary/hypothalamus disease) ↓ ↓ or normal
Hyperthyroidism ↑ ↓

550
Adrenal disorders
Acute adrenal insufficiency (adrenal crisis)

I. Description: results from lack of cortisol as caused by the following:

A. Too rapid cessation of steroid therapy

B. Stress, trauma, infection, surgery, or prolonged fasting in a patient
with Addison’s disease (i.e., insufficient amount of steroid therapy) C.
May occur as a result of pituitary destruction, bilateral adrenalectomy,
or trauma to adrenal glands
II. Signs and symptoms

A. The predominant feature is shock.

B. The patient often has nonspecific symptoms such as follows:
1. H/A and lassitude
2. N/V, anorexia
3. Fever
4. Hypotension and/or dehydration out of proportion to current illness 5.
Skin hyperpigmentation (with long-standing adrenal insufficiency) 6.
Weakness, fatigue, lethargy
7. May have confusion or coma
III. Treatment

A. Transfer immediately for emergency treatment

B. After acute crisis, maintenance doses of corticosteroids (may co-
manage with the physician)

Chronic adrenal insufficiency (addison’s disease)

I. Description: autoimmune destruction of adrenal cortices results in chronic cortisol,

aldosterone, and adrenal androgen deficiency II. Signs and symptoms

A. Hallmark signs are hypotension and hyperkalemia

B. Other signs may include the following:
1. Increased skin pigmentation and diffuse tanning (especially over
flexor surfaces, palm creases, and areolae) 2. Volume and sodium

551
 depletion
3. Chronic malaise
4. Generalized weakness and/or fatigue, worse with exertion and better
with bed rest 5. Anorexia, N/V, diarrhea
6. Scant pubic and axillary hair
7. Psychiatric
a) mild-to-moderate organic brain syndrome or memory impairment
b) depression
c) psychosis
III. Diagnostic tests

A. CBC: WBC shows moderate neutropenia, lymphocytosis, elevated

eosinophils B. CMP: hyperkalemia, hyponatremia, hypoglycemia
IV. Treatment

A. Refer to an endocrinologist
B. Replacement glucocorticoids and mineralocorticoids for life
C. The patient should be educated (by the endocrinologist) on how to
manage minor illnesses and major stresses and when and how to inject
glucocorticoids for emergencies D. The patient should wear an ID
band stating he/she has Addison’s disease

Cushing’s syndrome and disease

I. Description

A. Cushing’s syndrome: caused by adrenal hyperplasia or tumors,

extraadrenal malignancies, or chronic glucocorticoid use B. Cushing’s
disease: generally caused by ACTH hypersecretion due to pituitary
adenoma
II. Signs and symptoms (none are diagnostic and many are nonspecific)

A. Central (truncal) obesity

B. Moon face, buffalo hump, supraclavicular fat pads
C. Protuberant abdomen with purple striae, thin extremities
D. Oligomenorrhea or amenorrhea, impotence

552
 E. Weakness, especially in the upper arms, legs, and hips
F. Acne; thin skin with easy bruising and poor wound healing
G. Progressive weight gain
H. Labile mood to psychosis
III. Treatment

A. Refer to an endocrinologist if you suspect the condition

B. If appropriate, the patient should wear an ID band stating he/she has
Cushing’s syndrome or disease

Pheochromocytoma

I. Description: caused by tumor in the adrenal glands or sympathetic chain II. Signs and
symptoms

A. Triad of attacks of H/A, sweating, and tachycardia (paroxysmal, but

many patients do not have these together) B. Paroxysmal HTN
C. H/A, mild to severe
D. Generalized sweating
E. Weakness
F. Anxiety, tremor
G. Patients who have paroxysmal HTN and tachycardia during
diagnostic procedures, anesthesia, or surgery or with foods containing
tyramine should be evaluated for pheochromocytoma
III. Diagnostic tests: 24-hour urine for fractionated catecholamines, metanephrines, and
creatinine (all elevated); if positive, consider abdominal CT with and without oral and IV
contrast and pelvic CT without contrast IV. Treatment: refer to a surgeon with positive test
results

553
Diabetes mellitus
Categories (also see table 16-2)

I. Type 1: the pancreas produces no insulin

II. Type 2: insulin resistance; eventually insulin production decreases

A. DM or impaired glucose tolerance may develop as a result of the

following:
1. Pancreatic disease (e.g., cystic fibrosis or chronic pancreatitis) 2.
Endocrinopathy (e.g., Cushing’s syndrome, acromegaly, or
pheochromocytoma) 3. Drugs and chemical agents (e.g., thiazide
diuretics primarily at doses >25 mg HCTZ qd or equivalent,
glucocorticoids, atypical antipsychotics)
B. Gestational DM (GDM): develops during pregnancy (usually at 24 to
28 weeks’ gestation) owing to increased amounts of glucocorticoids
and other hormones released from the placenta; usually disappears
when pregnancy ends
III. Insulin resistance

A. Consider diagnosis with one or more of the following:

1. Presence of PCOS
2. Weight gain
3. Dyslipidemia
4. Systolic BP elevated after eating
5. Clotting abnormalities
6. Presence of nonalcoholic fatty liver disease (NAFLD)
7. Presence of diastolic dysfunction
a) S4 heart sound
b) possible HF
c) echo shows stiff left ventricle (secondary to free fatty acid [FFA]
deposits)
8. Gout (increased FFA deposits in kidneys interfere with uric acid
excretion)

554
 B. Evaluation
1. Elevated 2-hour value during GTT (Table 16-3), which indicates either
impaired glucose tolerance or type 2 DM
2. There is no validated clinical test to measure insulin resistance directly
IV. Prediabetes: fasting and/or 2-hour glucose higher than normal but not high enough to meet
the criteria for DM

A. Impaired fasting glucose: FBG 100 to 125 mg/dl

B. Impaired glucose tolerance: 2-hour glucose 140 to 199 mg/dl on GTT
Table 16-2
Overview of Type 1 and Type 2 Diabetes

Characteristic Type 1 Type 2

Usual age at Usually around puberty but Older than 30 years of age*
onset 25% present after 35 years of
age

Associated with Not usually Frequently

obesity

Classic signs and Polyuria, polyphagia, Relatively few classic symptoms

symptoms polydipsia Repeated or hard-to-heal vaginal yeast or bladder infections
Weight loss May have blurred vision, tingling in extremities, poor wound healing
Fatigue, weakness May have acanthosis nigricans
Feeling edgy, moody
Children may present:
Asymptomatically or
With DKA or only with ketonuria or
Symptomatically (BG >600 mg/dl, severe dehydration) but without
ketonuria or acidosis or Symptomatically (e.g., polyuria, polydipsia,
nocturia)

Etiology Beta-cell destruction because Genetic and environmental factors appear to be important
of autoimmune disease Usually arises because of insulin resistance combined with relative
Genetic and environmental insulin deficiency
triggers

Ketosis prone Yes No, except in periods of acute stress

Dependent on Yes No, may eventually require insulin therapy to control hyperglycemia
insulin to sustain
life

*
More children, even as young as 10 years, are being diagnosed with type 2 DM; this is probably related to lifestyle changes such as
increased fast food intake and decreased activity.

Table 16-3
Criteria for Diabetes, Prediabetes, and Gestational Diabetes

DM Pre-DM Gestational DM

555
 FBG levels ≥126 mg/dl on at
least two occasions* (preferred
test) Random blood glucose
≥200 mg/dl†
2-h value during GTT >200
mg/dl
A1c >6.5%
FBG levels 100-125 mg/dl on at least two After receiving a 100-g glucose load:
occasions* (preferred test) 2-h value during positive test result if two values meet or
GTT is 140-199 mg/dl (impaired glucose exceed the following: FBG levels: 105
tolerance) mg/dl
A1c 5.7%-6.4% 1-h GTT: 190 mg/dl
2-h GTT: 165 mg/dl
3-h GTT: 145 mg/dl

*Oral
GTT is not necessary if fasting glucose levels are elevated on two occasions.
†Order FBG and A1c to verify.

Screening

I. Adults aged >45 years; if normal, repeat testing q3yrs

II. Adults aged <45 years if overweight (BMI ≥25 kg/m2) AND one or more additional risk factors

A. First-degree relative with DM: parent, sibling, child

B. Member of a high-risk ethnic population: African American, Hispanic,
Native American, Asian American, or Pacific Islander C. Has delivered
a baby weighing >9 lb or has been diagnosed with GDM
D. Previously documented pre-DM
E. HTN: BP >140/90 mmHg
F. HDL levels <35 mg/dl or triglyceride levels >250 mg/dl or both G.
Habitual physical inactivity
H. History of vascular disease
I. Has other clinical conditions associated with insulin resistance (e.g.,
acanthosis nigrans, PCOS)
III. Screening for DM in children

A. Remains controversial because there are no data from controlled

studies showing that earlier diagnosis improves long-term outcomes B.
The ADA recommends: screening q3yrs in children (starting at 10
years of age) if overweight (BMI >85th percentile for age and sex) plus
any two of the following risk factors:
1. First-or second-degree relative with type 2 DM
2. Member of a high-risk ethnic population: non-Hispanic Black,
Hispanic, Native American, Asian American, or Pacific Islander 3.
Signs of or conditions associated with insulin resistance (e.g.,
acanthosis nigricans, HTN, dyslipidemia, or birth weight small for
gestational age) 4. Mother had DM or gestational DM during child’s

556
 gestation
C. Diagnostic criteria values are the same as for adults (see Table 16-3)
IV. Screening in pregnancy

A. Screen between 24 and 28 weeks’ gestation; give 50 g oral glucose load

and obtain plasma glucose 1 hour later (fasting not necessary); a value
of >140 mg/dl indicates the need for fasting 3-hour GTT
B. Screen as early as the first prenatal visit in women with a high risk of
GDM (e.g., marked obesity, past history of GDM, glycosuria, or strong
FH of DM); if this screening has negative results, repeat at 24 to 28
weeks’ gestation

Diagnosis

I. Diagnosis is based on the criteria set by the ADA; see Table 16-3 for specific criteria II.
Diagnosis of DM and pre-DM should be based on blood glucose values by laboratory
determination or A1c values and not by capillary blood glucose monitors

Initial office evaluation

I. History

A. Symptoms of DM (see Table 16-2) B. PMH

1. Eating patterns, nutritional status, weight history; growth and
development in children and adolescents 2. Current treatment:
medications, meal plan, self-monitoring of blood glucose (SMBG), and
patient’s use of data 3. Previous DM treatment, including nutrition and
self-management education 4. Prior A1c results
5. History and treatment of other conditions, including eating and
endocrine disorders
6. Gestational history and contraception
7. Frequency, severity, and causes of acute complications (e.g., DKA,
hypoglycemia) and prior or current infections (especially GU, skin,
foot, and dental) 8. Symptoms and treatment of chronic complications
of DM (see later in this chapter) 9. Risk factors for atherosclerosis (e.g.,
smoking, HTN, hyperlipidemia)
C. Social history
1. Exercise history

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 2. Tobacco, ETOH, and/or controlled substance use
3. Lifestyle, cultural, psychosocial, educational, and economic factors that
may influence DM management
D. Family history of DM and other endocrine disorders
II. Physical examination

A. Height and weight (growth chart for children and adolescents)

B. Sexual maturation (in the peripubertal period; see Tanner’s staging,
Box 2-1) C. Vital signs
D. Fundoscopic evaluation
E. Oral examination
F. Thyroid palpation
G. Cardiovascular, including auscultation for bruits and palpation of
pulses H. Abdominal examination
I. Skin examination (for acanthosis nigricans)
J. Neurological examination, including sharp and dull sensations
K. Foot examination (including monofilament for neuropathy) (Figure
16-1)
III. Diagnostic evaluation

A. Fasting complete chemistry panel and lipid profile

B. A1c
C. UA for glucose, ketones, protein, and evidence of microalbuminuria
or infection D. ECG (adults) at initial evaluation and then as indicated
IV. Referrals (if indicated)

A. Diabetes Education Program (this is a standard of care for DM,

recommended by the ADA and American College of Endocrinologists)
B. Dietitian consultation (especially if the patient is newly diagnosed);
if someone else in the home does meal planning and cooking,
encourage that person to attend the appointment; this is recommended
if it is not part of the Diabetes Education Program or as a follow-up
visit for further teaching or clarification C. Annual dilated eye
examination by an ophthalmologist or optometrist D. Podiatrist for
orthotics or evaluation/treatment of abnormal findings

558
 FIGURE 16-1 Monofilament Testing Sites on Feet. Source: (From Mosby:
Managing Major Diseases: Diabetes Mellitus and Hypertension, New York, 1998, Elsevier.)

Goals

I. The overall goals for management of DM are as follows:

A. Type 1
1. Avoid excessive hypoglycemia and hyperglycemia, especially when
accompanied by ketoacidosis 2. Balance food intake with insulin and
exercise
3. Maintain an appropriate weight and provide optimal nutrition
B. Type 2
1. Eliminate symptoms
2. Improve quality of life
3. Reduce the risk of microvascular and macrovascular complications
through glycemic control
II. Individualize the goals, taking into account the patient’s ability to understand and carry out
the treatment regimen and understand the risk of hypoglycemia III. Emphasize that DM is a
chronic disease and management of it involves four equal tools

A. Meal plan
1. Diet management is of utmost importance; poor eating habits will

559
 lessen or negate efforts to achieve lower blood glucose levels 2. Weight
reduction when indicated
a) any degree of weight loss is likely to improve blood glucose levels
and/or decrease the need for medications b) can also improve liver
function in nonalcoholic fatty liver disease, which is associated with
insulin resistance and type 2 DM
3. See also CURRENT DIETARY RECOMMENDATIONS below
B. Lifestyle changes
1. Exercise (see EXERCISE AND DIABETES, later in this chapter) 2. Quit
smoking
3. Noncardiac benefits may include reduction in urinary incontinence,
OSA, and depression; may also improve mobility and physical
conditioning
C. Monitoring
1. Blood glucose goals
a) 70 to 130 mg/dl fasting or preprandial; <180 mg/dl hs or 1 to 2 hours
postprandial b) A1c: should be tailored by balancing improved
complications with the risk of hypoglycemia; reasonable is <7% (or
<6.5% if done safely) but in older patients or those with limited life
expectancy or comorbid conditions, strive for <8%
2. Maintain BP <140/90 mmHg
3. Control hyperlipidemia if necessary; suggested priority is as follows:
a) LDL (see Chapter 8, Hyperlipidemia) b) HDL >40 mg/dl (males) or >50
mg/dl (females)
c) Triglycerides <150 mg/dl
D. Medications (if needed) (see Figure 16-3)
IV. For patients with pre-DM: emphasize the risk of developing actual DM unless lifestyle
changes are made

A. The best results follow changes in eating, similar to DM; it is a good

idea to have the patient meet with a dietitian knowledgeable about
DM
B. Encourage the patient to work up to walking 30 minutes 5 times a
week; it can be split into two 15-minute walks if this is more feasible.

560
 Walking should be faster than a casual stroll, but the patient is still
able to carry on a conversation without difficulty.
C. Weight reduction is an important goal (see Nutritional goals below)

Current dietary recommendations

I. Nutritional goals

A. Maintain as near-normal blood glucose as possible by balancing food

intake with activity and medications (as needed) B. Control BP and
lipids
C. Provide adequate calories to achieve and maintain a healthy body
weight; to calculate the desired body weight (±10%, depending on
frame size)
1. Women: 5 feet = 100 lb; add 5 lb for each additional inch of height and
subtract 5 lb for each inch less than 5 feet 2. Men: 5 feet = 106 lb; add 6
lb for each additional inch
D. If weight loss is indicated (BMI ≥25 kg/m2), encourage the patient to
set a goal of losing 5% of the body weight (not so overwhelming as a
goal of losing ≥50 lbs)
1. Calorie restriction (e.g., 500 fewer calories qd) will result in short-term
blood glucose improvement 2. Long-term blood glucose control also
requires weight loss
3. There is no general consensus on the best weight loss plan; some
examples are as follows:
a) counting calories
b) replacing two meals and one or two snacks with meal replacement
shakes or bars (for weight loss); replacing one meal and one snack (for
weight maintenance) c) low carb diet
d) Mediterranean diet
II. ADA recommendations for food planning in DM

A. Encourage carbs from fruits, vegetables, whole grains, legumes, and

low-fat milk B. With carbs: use of glycemic index and glycemic load
may help with blood glucose control C. Saturated fat <7% of the total
calories; minimize trans fat intake D. Total cholesterol <200 mg daily

561
 E. Protein
1. 15% to 20% of total calories daily (if no significant renal insufficiency)
2. 0.8 to 1 g/kg body weight daily (with early stages of CKD)
F. Fiber: at least 14 g per 1000 calories daily
G. Sugar alcohols (e.g., sorbitol) have a low glycemic effect but may
cause diarrhea H. Noncaloric sweeteners approved by the FDA are
acceptable
III. Teach the patient how to make adjustments for hyperglycemia, hypoglycemia, illness, and
exercise (especially when on insulin therapy) IV. Alcohol

A. Avoid in people with poor metabolic control, those attempting weight

loss, those with elevated triglycerides, those with nephropathy, and in
pregnant women B. Moderate intake (1 to 2 servings per day for men;
1 per day for women) is acceptable; 1 drink = 12 oz beer = 5 oz wine =
1.5 oz 80-proof liquor C. Can contribute to hypoglycemia in patients
taking insulin or sulfonylureas; for this reason, recommend that the
patient eat protein when drinking alcohol
V. Micronutrients

A. Sodium: <1500 mg qd
B. Potassium
1. Increase intake in patients taking diuretics that are not potassium
sparing 2. Restrict in patients with renal insufficiency and those taking
ACEs or ARBs
VI. Supplements

A. Vitamins and minerals are generally not needed if the patient has
adequate dietary intake B. Chromium has been shown to improve
blood glucose control in some randomized trials involving patients
with DM
C. Cinnamon: studies have shown conflicting results regarding its
effectiveness in DM; none have shown harm
VII. Meal planning strategies

A. The plan should be appropriate for the patient’s lifestyle and should
provide day-to-day consistency in calorie and carbohydrate intake and
mealtimes; update as needed for changes in growth or lifestyle;
encourage these guidelines:

562
 1. Eat three balanced meals qd, 4 to 5 hours apart
2. Eat at the same time qd whenever possible
3. Include a bedtime snack, especially if taking insulin
4. Avoid high-sugar foods and drinks
B. SMBG data should be used to make adjustments in food intake or
insulin dosages C. The exchange list is only one method of meal
planning; the point system, carbohydrate counting, plate method
(Figure 16-2), and others may also be used D. The most important
dietary component is for the patient to learn to estimate the amount of
carbs they are eating in any meal or snack (especially if on insulin
therapy)

FIGURE 16-2 The Plate Method. Source: (Using a Standard Size Dinner Plate).

Exercise and diabetes

I. Important elements for both types of DM are listed in Table 16-4

563
II. Weight loss and exercise work together to decrease insulin resistance, which is a primary
problem in type 2 DM
III. Exercise can also delay progression of impaired glucose tolerance to type 2 DM
IV. Individualize the exercise plan according to the patient’s level of fitness, lifestyle, and
motivation

A. Warm-up and cool-down for 5 to 10 minutes (walk at a comfortable

pace; gentle stretching) B. Keep moving (i.e., aerobic activity) for 20 to
30 minutes; the patient may have to work up to this. The goal is 30
minutes on most days of the week.
C. No matter what the activity, the patient should be able to talk without
SOB
D. Wear proper shoes; check feet before and after exercise
E. Drink plenty of water to avoid dehydration
1. Two hours before exercise: two cups
2. Thirty minutes before exercise: one to two cups
3. Every 15 mins during exercise: one half cup
F. Patients may need extra food for up to 24 hours after exercise,
depending on the duration and intensity of workout
V. Exercise restrictions

A. Avoid exercise in extreme heat or cold and during periods of poor

glycemic control B. Active proliferative retinopathy: any type of
resistance training (e.g., free weights or weight machines)
C. Peripheral neuropathy: avoid weight-bearing activities (e.g., running,
prolonged downhill skiing) D. HTN: avoid activities that involve
straining
VI. Exercise points for patients using insulin (Table 16-5)

A. Do not exercise if the blood glucose level is <60 mg/dl or >250 mg/dl B.
Always begin exercise at least 1 hour after the last insulin injection and
avoid exercise during the time of peak insulin action C. Encourage the
patient to have a quick snack readily available (see Table 16-11,
Treatment of Hypoglycemia) D. If hypoglycemic symptoms occur
during exercise, stop immediately and check blood glucose levels
Table 16-4
Exercise and Diabetes

564
 Type 1 DM Type 2 DM
Potential Cardiovascular Cardiovascular
benefits of
exercise • Decreased VLDL and triglycerides • Decreased VLDL and
• Increased HDL triglycerides

• Decreased BP • Increased HDL

• Increased cardiac work capacity • Decreased BP

Weight control • Increased cardiac work

Decreased stress capacity
Improved sense of well-being Assists with weight loss and
maintenance
Increased insulin sensitivity
Improved blood glucose control by
increasing insulin sensitivity
Reduced need for insulin or OHAs
Improved quality of life
Decreased stress
Improved sense of well-being

Potential Hypoglycemia can be delayed or prolonged after extended or
risks and intense exercise Arrhythmias or MI can be precipitated in
precautions patients with cardiovascular disease Some types of exercise
may worsen retinopathy and may lead to problems in patients
with neuropathy
Cardiovascular, ophthalmologic, and
neurovascular complications are relative
contraindications or precautions to
exercise

Medical Assess glycemic control (e.g., A1c) Assess glycemic control (e.g., A1c)
evaluation Cardiovascular examination Cardiovascular examination (BP, pulses,
before bruits, blood lipids, ECG if the patient is
initiation of Neurological and musculoskeletal examinations, including
examination of feet Ophthalmoscopic examination older than 35 years or has a history of a
an exercise cardiovascular disease) Graded exercise
program* treadmill
Neurological examination
Ophthalmoscopic examination
*
With abnormal findings, refer to Exercise restrictions, below.

Table 16-5
Food and Insulin Adjustments for Exercise

Variable Management and Adjustment

Blood Glucose Levels
<100 mg/dl Add a snack and recheck glucose in 15-30 min

≥250 mg/dl Adjust insulin

Delay exercise until glucose decreases

Exercise
Moderate exercise for <30 mins No snack unless blood glucose level is <80 mg/dl

Exercise for >30 mins A snack every 30-60 mins

The snack should be ∼10-15 g of carbohydrates for every 30 mins of exercise (see Table
16-11)*

Strenuous exercise for >45-60 May require <20% decrease in the corresponding insulin component

565
 mins Do not inject insulin into the exercising extremity

Prolonged rigorous exercise May require large decreases in insulin (⅓ to ½ of the usual dose)

*The
snack size may vary from patient to patient and with the duration and intensity of exercise.

Monitoring

I. SMBG

A. All patients with DM who use insulin or other DM medications that

can cause hypoglycemia should perform SMBG
B. Monitoring may vary with the following:
1. Level of glycemic control desired
2. Medication regimen variations
3. Propensity for hypoglycemia
4. More frequent testing is necessary when the usual daily schedule is
changed (e.g., travel, surgery, hospitalization) or during periods of
illness or stress 5. Type of DM
a) type 1 on multiple-dose insulin or insulin pump
(1) before meals and snacks and at hs
(2) occasionally postprandial
(3) before exercise
(4) when hypoglycemia is suspected or after treatment for low blood
glucose (until glucose levels are normal) (5) before driving or
operating machinery
b) type 2
(1) frequency depends on glycemic goals and treatments used
(2) may motivate the patient to make lifestyle changes but is expensive
(3) may not be needed for patients who are managed with diet and/or
oral agents not associated with hypoglycemia
C. Tips for effective SMBG
1. 1-or 2-hour postprandial testing may be helpful 2 to 3 times a week
(allows the patient to see the effects of a particular type of food on
blood glucose levels)

566
 2. Patients with nocturnal hypoglycemia should test 1.5 to 2 hours after
the evening snack or between 1 and 3 am once or twice a week 3. The
patient should record all test results. Recording insulin doses (when
applicable) along with the blood glucose results is also helpful; be sure
that the patient knows that he/she must separately enter routine doses
and compensatory doses (e.g., according to a “sliding scale”).
4. Teach the patient to record results in a method that allows quick
comparison of day-to-day results so that the patterns are easily
recognizable 5. The patient should know how to respond
appropriately to SMBG results by making adjustments in the diet or
insulin regimen; the goal is to achieve and maintain blood glucose
levels within the desired range individualized for each patient (Table
16-6)
II. Glycosylated hemoglobin (A1c)

A. Best method for assessing long-term glucose control because it reflects

mean blood glucose concentration over the preceding 8 to 12 weeks
(previous month accounts for ∼50% of the A1c value). An A1c of 6
corresponds to an average blood glucose of 125 mg/dl; every increase
in A1c of 1 point (e.g., changes from 6 to 7) corresponds to an increase
in average blood glucose of 30 mg/dl.
B. Not affected by glucose at the time the specimen is drawn, so fasting is
not necessary C. With discrepancies between SMBG and A1c
1. Inaccurate testing technique or machine malfunctioning
2. Fabricated SMBG results
a) A1c 7% to 8.4%: much of the problem is increased FBG
b) A1c >8.4%: much of the problem is postprandial sugars
3. Inappropriate timing of SMBG
4. Hemoglobinopathies (e.g., sickle cell anemia lowers results;
hemoglobin F may elevate results)
5. A1c represents an average blood glucose concentration, so fluctuations
in blood glucose levels may result in near-normal A1c levels
III. Follow-up office evaluations

A. Frequency

567
1. Every 3 months in type 1 DM or uncontrolled type 2 DM
2. Every 4 to 6 months in controlled type 2 DM
3. Every 6 months with pre-DM
B. History
1. Frequency and cause(s) of hypoglycemic and hyperglycemic episodes
2. Results of SMBG
3. Any changes by the patient in the treatment plan; problems with
adherence 4. Symptoms suggesting development of complications of
DM
5. Current medications
6. Psychosocial issues (e.g., quality of life issues, depression, ability to
pay for medications or tests)
C. Physical examination
1. Height and weight
2. BP
3. Cardiovascular examination including bruits and pulses
4. Oral examination for periodontal disease
5. Foot examination
D. Laboratory and other testing
1. Complete chemistry profile (at least q3-6mos)
2. A1c
a) q3mos in type 1 DM or type 2 DM with poor glycemic control
b) q6mos if the patient has stable glycemic control or in a patient with
pre-DM if FBG levels remain above normal
3. Annual fasting lipid profile, urinalysis for protein and albumin-to-
creatinine ratio, TSH (as indicated) 4. Annual dilated eye examination
by an ophthalmologist or optometrist
E. Counseling
1. Discuss treatment goals and plan
2. Review food plan

568
 3. Discuss exercise and weight reduction plan (if indicated)
4. Review medications
5. With poorly controlled DM, consider the following:
a) overeating (specifically, simple carbs)
b) inadequate exercise and/or activity
c) overinsulinization (usually in patients with marked “glucose
bounces”) d) incorrect insulin injection (technique and/or sites)
e) overeating carbs at night in response to minor hypoglycemia
symptoms f) chronic ETOH use with an underlying hepatic disease
g) eating disorders
h) depression and/or anxiety disorders
IV. Referral (to an endocrinologist)

A. Concurrent illness (e.g., infection or dehydration requiring

hospitalization) B. Diabetic ketoacidosis
C. Recurrent hypoglycemia
D. Unable to obtain glycemic control
Table 16-6
Suggested Adjustments with Blood Glucose Excursions

Blood
Insulin
Glucose Diet Adjustments Additional Points
Adjustments
Value
<50 mg/dl Include at least 10 g of Give injection Recheck blood glucose level 30-60 mins after the meal to
quick carbohydrates right before the ensure it is in the normal range
during the meal meal
Decrease
insulin* by 2-3
units

50-70 None Give injection Recheck blood glucose level 30-60 mins after the meal to
mg/dl right before the ensure it is in the normal range
meal
Decrease
insulin* by 1-2
units

70-130 None None

mg/dl

130-150 None Increase

mg/dl insulin* by 1

569
 unit

150-200 None Increase Recheck blood glucose level 1-2 h after the meal to ensure it is
mg/dl insulin* by 2 in the normal range
units

200-250 Delay the meal ∼45 mins Increase Recheck blood glucose level 1-2 h after the meal to ensure it is
mg/dl after injection insulin* by 3 in the normal range If pregnant, check urine for ketones with
units blood glucose level >200 mg/dl

250-300 Delay the meal ∼45-60 Increase Recheck blood glucose level 1-2 h after the meal to ensure it is
mg/dl mins after injection insulin* by 4 in the normal range
Increase fluid intake if units
urine ketones are
moderate to large

300-350 Delay the meal ∼45-60 Increase Recheck blood glucose level in 2-3 h
mg/dl mins after injection insulin* by 5
Increase fluid intake if units
urine ketones are
moderate to large

350-400 Delay the meal ∼45-60 Increase Recheck blood glucose level in 2-3 h
mg/dl mins after injection insulin* by 6
Increase fluid intake if units
urine ketones are
moderate to large

>400 Delay the meal ∼50-60 Increase Recheck blood glucose level in 2-3 h
mg/dl mins after injection insulin* by 7
Increase fluid intake if units
urine ketones are
moderate to large

Any Planned meal is larger Increase Recheck blood glucose level in 2-3 h
blood than usual insulin* by 1-2 Recheck blood glucose level in 2-3 h
glucose Planned meal is smaller units
value Recheck blood glucose level in 2-3 h
than usual Decrease
insulin* by 1-2 If insulin is adjusted, recheck blood glucose level in 2-3 h
Unusually increased
activity after a meal: eat units
extra carbohydrates Decrease
Unusually decreased insulin* by 1-2
activity after a meal units
Consider
increasing
insulin* by 1-2
units

*
Short-acting or rapid-acting insulin.

Medical therapy

I. Type 1 DM requires insulin (see Insulin therapy [IV in this section]) as well as dietary
management II. Treatment of type 2 DM involves lifestyle changes plus medication

A. Instituting treatment early in the course of DM, before A1c is

570
 significantly elevated, is associated with improved glucose control and
decreased long-term complications B. Consider initiating metformin
along with lifestyle changes (Figure 16-3) C. Interventions should be
changed if A1c is not at goal (see Goals, Monitoring, earlier in this
chapter) D. Other medications may be given as indicated (see Table 16-
7 for Suggested Hypoglycemic Agents)
III. Noninsulin hypoglycemic agents

A. Oral hypoglycemic agents (OHAs) are ineffective unless a DM food

plan, weight loss (as appropriate), and exercise are part of the
management plan; in reality, these are more effective than OHAs for
decreasing insulin resistance B. Taking an “extra” dose of OHAs to
cover excess food intake is ineffective and may be harmful; this should
be emphasized to patients C. Reinforce that OHAs are not oral insulin
and do not work like insulin D. When one OHA is being changed for
another, a delay between regimens is not necessary E. There are very
few comparison trials of available agents, so the choice is often based
on any underlying conditions (e.g., renal insufficiency, HF), cost of
medication(s), and patient preferences
F. DPP-4 inhibitors, GLP-1 receptor agonists, α-glucosidase inhibitors,
and SGLT2 inhibitors (Table 16-8) are usually not recommended as
monotherapy or first-line therapy G. Pioglitazone is usually not first-
line therapy
H. In patients intolerant to or unable to take metformin or sulfonylureas,
repaglinide or pioglitazone are reasonable alternatives I. Likely weight
effects
1. Gain: pioglitazone, sulfonylureas, meglitinides, insulin
2. Loss or no change: metformin, GLP-1 receptor agonists, α-glucosidase
inhibitors, DDP-4 inhibitors
J. Possible causes for OHA failures
1. Overeating and weight gain
2. Poor compliance
3. Lack of physical activity
4. Stress or concurrent illness (e.g., surgery, trauma, infection) 5.
Decreasing beta-cell function or increasing insulin resistance

571
 6. Inadequate drug dosage
7. Concomitant therapy with diabetogenic drugs (e.g., corticosteroids)
K. Management of OHA failures
1. Address possible causes before altering therapy
2. Combination therapy (e.g., with metformin) may be more successful
than monotherapy 3. Insulin may “tune up” insulin receptors initially,
after which, use of an OHA may be effective 4. Most patients require
insulin after 10 to 15 years of OHA therapy because of declining beta-
cell function
IV. Insulin therapy

A. Indications
1. Type 1 DM: provide insulin to cover basal insulin secretion and
postprandial glucose excursions 2. Type 2 DM
a) hyperglycemia and unable to achieve A1c <8.5% despite lifestyle
changes and noninsulin agents b) pregnancy
c) periods of stress, illness, or injury
d) marked and otherwise unexplained recent weight loss and/or
presence of moderate-to-heavy ketonuria e) onset of chronic
complications
f) newly diagnosed with A1c >10%
B. Pharmacokinetics of insulin: optimal insulin therapy requires an
understanding of insulin pharmacokinetics; see Tables 16-9 and 16-10
C. Initiating insulin
1. Type 1 DM
a) total daily dose (TDD) is 0.3 to 1 units/kg/day (start with 0.3 units/kg)
b) 40% to 50% of the TDD is the basal requirement; it should be NPH
bid (two thirds of the dose in the morning and one third at hs) or
glargine or detemir once or twice daily c) the rest of the TDD is short-
or rapid-acting insulin divided among mealtimes; individual doses
will depend on preprandial glucose readings and meal size d) when
adjusting the insulin dose, start conservatively (e.g., 1 unit for every 50
mg/dl glucose above/below desired and titrate as needed); on average,
1 unit of short-acting insulin will lower blood glucose levels 20 to 70

572
 mg/dl e) once-daily dose of glargine or detemir alone will rarely
control hyperglycemia in type 1 DM
2. Type 2 DM
a) assess lifestyle, willingness to start insulin, and blood sugar data b) a
common combination is once-daily insulin added to an existing OHA
regimen
(1) use NPH or detemir at hs or glargine in the morning
(2) the starting dose is 10 units/day; adjust according to self-monitored
FBG results (3) for suggested titration: increase the insulin dose by 3
units q3d as long as the average FBG is >130 mg/dl (4) the titration can
be more aggressive if FBG levels are >250 mg/dl
c) if starting preprandial insulin, use rapid-or short-acting insulin and
start with 5 units before the largest meal of the day; adjust according to
blood glucose readings (e.g., by 2 units q3d) d) it may take ≥100 units
of insulin qd for obese patients to achieve near-normal glucose goals
D. Insulin regimens
1. The goals of insulin therapy are as follows:
a) fasting glucose <130 mg/dl
b) preprandial glucose 70 to 130 mg/dl
c) bedtime glucose <140 mg/dl
2. Conventional insulin therapy: two injections daily
a) mixture of rapid-or short-acting and NPH insulin before breakfast and
supper; fasting hyperglycemia is often a problem; this can often be
corrected by giving evening NPH at hs, rather than with presupper
rapid-or short-acting insulin (this means more than two injections/day)
b) requires strict timing of the meal and snack schedule to avoid
hypoglycemia c) recommended dosing
(1) start with two thirds of the total daily dose in the morning and one
third of the dose in the evening; morning dose: one third of the total
dose as rapid-or short-acting insulin and two thirds as NPH
(2) evening dose: half of the total dose as rapid-or short-acting insulin
and half as NPH; some clinicians use the same ratio as the morning
dose (3) children: often closer to 20% rapid-or short-acting insulin and

573
 80% NPH for both morning and evening doses
3. Intensive insulin therapy: three injections daily
a) indicated in type 1 DM and in severely insulin-deficient type 2 DM
(when once-or twice-daily injections have not been successful) b)
requires greater effort by the patient to coordinate diet, activity, insulin
administration, and SMBG
c) recommended dosing
(1) two thirds of the total dose in the morning; remaining one third split
between presupper and hs doses (2) the morning dose is short-or
rapid-acting insulin and NPH
(3) the presupper dose is short-or rapid-acting insulin; the hs dose is
NPH
4. Intensive insulin therapy: multiple daily injections
a) basal insulin may be NPH, glargine, or detemir at bedtime
b) short-or rapid-acting insulin preceding each meal to correct
postprandial excursions; short-acting insulin is taken 30 minutes ac
and rapid-acting insulin is taken immediately ac c) Suggested
adjustments for preprandial blood glucose reading

If blood glucose is: Increase premeal insulin by:

130-160 mg/dl 5 units
161-200 mg/dl 8 units
201-240 mg/dl 12 units
241-280 mg/dl 16 units
281-320 mg/dl 20 units
>321 mg/dl 25 units

5. Advantages of intensive insulin therapy

a) increased flexibility in the timing of meals
b) adjustments for the size of meals are readily made
6. Disadvantages of intensive insulin therapy
a) requires frequent SMBG
b) fear of hypoglycemia
c) weight gain more likely
7. ADA guidelines for mixed insulin

574
 a) patients well controlled with a self-mixed regimen should continue as
they are (i.e., do not change to premixed insulin) b) glargine and
detemir should not be mixed together with other insulins c) after
mixing NPH with short-acting (i.e., regular) insulin, inject immediately
d) after mixing NPH with rapid-acting insulin, inject within 15
minutes before a meal
8. Continuous subcutaneous insulin infusion (CSII)
a) “pump” therapy provides insulin through tubing connected to a
subcutaneous catheter; a refillable cartridge holds enough short-or
rapid-acting insulin for about 2 days b) CSII also requires an expert
DM management team and availability of 24-hour support
E. Adjusting insulin
1. Before changing the insulin dose, determine the cause of
hypoglycemia or hyperglycemia if possible 2. Short-term adjustments
of the insulin dose consist of changes in the short-acting insulin
component (see Table 16-6) 3. Consistent elevations of blood glucose
levels at the same time qd for consecutive 2 to 3 days that cannot be
explained by changes in the diet or activity or by illness or stress can
be addressed by changes in the insulin component relevant to that
time period (see Table 16-10) 4. Change the basal dose by 3+ units at a
time and wait at least 3 days before changing it again; see Initiating
insulin, Type 2 DM

P r a c t i c e Pe a r l s f o r I n s u l i n T h e r a p y

• As a rule, normalize fasting blood glucose levels before normalizing the levels throughout
the remainder of the day (“fix the fasting first”).
• Reassure the patient that starting insulin is not a personal “failure”; most patients with type
2 DM will eventually need insulin because of a decline in insulin production.
• Intensive insulin therapy is contraindicated when

• The patient cannot comply with the regimen

• The patient is insensitive to signs of hypoglycemia
• The patient has seizures or compromised mental status
• Comorbid conditions, such as stroke or cerebrovascular disease, are

575
 present
• With variable blood glucose readings, consider the following:

• Absorption is reduced with increasing insulin doses; may try splitting

the amount of each injection into two separate sites.
• Site variability and absorption: fastest absorption from the abdominal
wall, slowest from the leg and buttock, intermediate from the arm; may
try preprandial regular or rapid-acting insulin injected in the
abdominal wall and evening NPH into the leg or buttock • To avoid
deficient insulin absorption because of fibrosis, recommend rotating to
a different site after 5 to 7 injections.
• Comparing glargine and detemir insulins

• They achieve similar A1c with similar rates of hypoglycemia.

• Detemir causes less weight gain but may require a higher daily dose,
divided bid.
• Converting NPH to longer-acting basal insulin (e.g., glargine or detemir)

• If NPH is once qd, use the same dose of longer-acting insulin.

• If NPH is bid, decrease the longer-acting dose by 20% (of the NPH
dose) initially.
• Converting longer-acting basal to NPH

• Convert unit for unit.

• NPH at hs, with oral medication in the morning or split the NPH dose
between morning and evening
• Teach the patient signs and symptoms of hypoglycemia, how to treat them, and what to do
on sick days (see Sick Day Management, later in this chapter).

576
 FIGURE 16-3 Suggested Therapy for Type 2 DM.
Table 16-7
Patient-Specific Suggested Noninsulin Hypoglycemic Agents

Patient Profile Suggested Agent Agents to Avoid

Elderly Glipizide or glimepiride Glyburide (or use at a lower dose)
Pioglitazone

Hepatic insufficiency Insulin Metformin

α-Glucosidase inhibitors
Meglitinides
Glipizide (or use at a lower dose)
Glyburide
Pioglitazone

Renal insufficiency Meglitinides Metformin

Pioglitazone α-Glucosidase inhibitors
DDP-4 inhibitors* Glyburide
GLP-1 agonists†

577
 Obese Metformin Sulfonylureas
GLP-1 agonists†

Age <18 years Metformin Meglitinides

Irregular schedule or eating habits α-Glucosidase inhibitors Sulfonylureas (hypoglycemia is more likely)
Pioglitazone
Meglitinides

Hyperlipidemia Metformin
Pioglitazone

Also taking insulin Pioglitazone (cautiously)

Metformin

HF Insulin Metformin
Pioglitazone

Postprandial hyperglycemia Meglitinides

*Dipeptidyl
peptidase-4 (DPP-4) inhibitors.
†Glucagon-like
peptide-1 (GLP-1) receptor agonists.

Table 16-8
Noninsulin Hypoglycemic Agents

Medication Action Administration Cautions & Contraindications

Secretagogues
Sulfonylureas: Second Generation
Glyburide Effective only Monotherapy or in Do not use two sulfonylureas simultaneously
(DiaBeta, with endogenous combination with insulin May cause severe hypoglycemia and weight gain
Glynase, insulin secretion or any of the other oral
Micronase) Contraindications
Increases beta-cell hypoglycemic agents Give
Glipizide insulin 30 min before breakfast Type 1 DM
(Glucotrol, production and (qd dosing) or 30 mins
Pregnancy or lactation
Glucotrol XL) secretion before breakfast and the
evening meal (bid dosing) Major surgery
Glimepiride Effective for 7-10
Severe infection, illness, trauma
(Amaryl) yrs in most
patients History of severe reaction to sulfa

Decreases A1c
1%-2%

Meglitinides
Nateglinide Stimulates insulin Monotherapy or in Do not use nateglinide in patients with impaired renal
(Starlix) release from combination with function
Repaglinide pancreas (glucose metformin May cause hypoglycemia and weight gain (less risk
(Prandin) dependent) Take within 30 mins of with repaglinide)
Decreases A1c starting the meal; do not Contraindications
0.5%-1.5% take if skipping the meal
(repaglinide more Ketoacidosis
effective) Type 1 DM
Pregnancy
Gemfibrozil used with repaglinide

Biguanides

578
Metformin Decreases hepatic Monotherapy or in May cause gastric distress or diarrhea, but these
(Glucophage, production of combination with insulin decrease with time
Glucophage glucose or other hypoglycemic Stop drug 48 h before surgery or any test with an iodine
XR) Enhances glucose agents contrast dye
uptake by muscle Give with meals; the
Monitor for symptoms of lactic acidosis (e.g., malaise,
extended-release tablets
Decreases LDL myalgias, respiratory distress, increased somnolence,
are taken once daily,
and triglyceride nonspecific abdominal distress) Can lower vitamin B12
regardless of how many
levels levels; check with anemia or if symptoms of peripheral
are taken
Not associated neuropathy develop Contraindications
with Type 1 DM
hypoglycemia Renal dysfunction (creatinine >1.5 mg/dl in males or
and weight gain >1.4 mg/dl in females) Pregnancy and lactation
Decreases A1c Alcohol abuse
1%-2%
Acute or chronic metabolic acidosis

α-Glucosidase Inhibitors
Acarbose Inhibits small Monotherapy or in High incidence of GI side effects (e.g., diarrhea,
(Precose) intestine enzymes combination with flatulence, cramping), especially if the meal is high in
Miglitol that break down sulfonylureas, metformin, carbohydrates or drug started at a comparatively high
(Glyset) complex or insulin dose Delays absorption of sucrose but not glucose; if the
carbohydrates Take with the first bite of patient is also taking insulin or sulfonylureas and
into the meal experiences hypoglycemic symptoms, give glucose tabs
monosaccharides or gel; candy, soda, or sugar-sweetened juices will not
Prevents help Contraindications
postprandial Ketoacidosis
glucose peak
Inflammatory bowel disease
No hypoglycemia
because there is Intestinal obstruction
no systemic Cirrhosis
absorption
Renal dysfunction (serum creatinine >2 mg/dl)
Decreases A1c
0.5%-0.8%

Glitazone
Pioglitazone Increases insulin Monotherapy or in Monitor LFTs q2mos for 12 mos, then periodically; stop
(Actos) sensitivity and combination with the drug if ALT levels are 3 times the upper limit of
decreases insulin sulfonylureas, metformin, normal Increased risk of hypoglycemia if used with
resistance or insulin insulin or sulfonylureas
Enhances glucose Increase the dose after 4 Monitor for signs of edema or HF and stop the drug at
transport into wks if necessary the first signs
cells Associated with weight gain and edema (especially at
Decreases higher doses)
triglycerides and Contraindications
increases HDL
levels Active liver disease

Decreases A1c History or diagnosis of HF

0.5%-1.4% Type 1 DM

GLP-1 Receptor Agonists

Exenatide Stimulates insulin Sub-q administration, in Possible link to pancreatitis
(Byetta, secretion when conjunction with Possible risk of medullary thyroid cancer
Bydureon) glucose levels metformin or
increase sulfonylureas Pay attention to dosing frequency (varies from bid to
Liraglutide once weekly, depending on medication)
(Victoza) Increases satiety
Albiglutide Decreases A1c
(Tanzeum) 1%-1.5%

579
 Dulaglutide
(Trulicity)

DDP-4 Inhibitors
Sitagliptin Slows Oral therapy, as Possible link to pancreatitis
(Januvia) degradation of monotherapy or in
Saxagliptin natural GLP-1, combination with
(Onglyza) thus enhancing metformin or
native GLP-1 sulfonylureas
Linagliptin effects (see GLP-1
(Tradjenta) Receptor
Agonists, above)
Decreases A1c
0.5%-0.8%

SGLT2 Inhibitors
Canagliflozin Increases urine Oral therapy, considered May lead to increased urination and possible
(Invokana) excretion of AFTER other second-line dehydration, UTIs and genital yeast infections Small
Dapagliflozin glucose options increased risk of bladder cancer with Farxiga
(Farxiga) Decreases A1c Avoid Farxiga and lower dose of Invokana with eGFR
Empagliflozin 0.7%-1% <60 ml/min; avoid Invokana or Jardiance with eGFR <45
(Jardiance) ml/min

Table 16-9
Pharmacokinetics of Insulin

Type of Insulin Onset Peak Effect Duration

Rapid-or Short-Acting
Insulin lispro (Humalog) 5-15 mins 45-75 mins 2-4 h
Insulin aspart (Novolog) 5-15 mins 45-75 mins 2-4 h
Regular (Humulin R, Novolin R) ∼30 mins 2-4 h 6-8 h
Basal
Intermediate-Acting
NPH (Humulin N, Novolin N) ∼2 h 4-12 h 12-18 h
Longer-Acting
Detemir (Levemir) ∼2 h 3-9 h 6-24 h*
Glargine (Lantus) ∼2 h None ∼24 h
*
Dose-dependent; higher dose (≥0.8 units/kg body weight) is associated with longer duration.
Combination insulins are also available; their pharmacokinetics depend on the individual components:
• 70/30 (NPH and Humulin regular)
• 75/25 (lispro protamine and insulin lispro)
• 70/30 (aspart protamine and insulin aspart)

Table 16-10
Pharmacokinetics of Split or Mixed Injections

Type of Insulin Peak Time Blood Glucose Affected

Morning short-acting Between breakfast and lunch Prelunch
Morning intermediate-acting Between lunch and supper Presupper
Evening short-acting Between supper and bedtime Bedtime
Evening intermediate-acting Overnight Morning fasting

580
Children & adolescents with type 2 DM (differences from care of
adults with type 2 DM)
I. Nutrition

A. Provide a diet that decreases calories and avoids sugar-containing soft

drinks but includes adequate nutrition for normal health and growth
B. The diet should not be limited to the child but should also include
other family members
II. Weight goals

A. The decision for weight reduction or weight maintenance depends on

the age of the patient, degree of obesity, and presence of other
comorbidities B. Initially, recommend that the patient and family
maintain the current weight (e.g., for 1 to 2 months). Once this is done,
they can then begin changes for weight loss.
C. The weight loss goal is BMI <85th percentile
1. Prepuberty: 0.5 kg/mo
2. After puberty: up to 0.5 to 1 kg/wk
D. Suggestions to consider
1. Smaller portion sizes
2. Substitute fruits and vegetables for carbohydrate-rich foods
3. Replace soft drinks and juices with water or calorie-free liquids 4. Eat
out less often
III. Physical activity

A. Initially, decrease the amount of sedentary time (e.g., watching TV,

playing video or computer games) B. Children with BMI ≥95th
percentile should primarily perform non–weight-bearing activities
(e.g., swimming, biking, short walks)
IV. Pharmacology

A. Only insulin and metformin are FDA-approved for use in children;

however, sulfonylureas and meglitinides have been used B.
Recommend multivitamin qd if taking metformin because of possible
impaired absorption of B12 and/or folic acid

Hypoglycemia

581
I. Definition: blood glucose levels <50 to 60 mg/dl
II. Possible causes

A. Relative insulin excess inhibits hepatic glucose production and

stimulates glucose utilization by muscle and fat tissue B. Increase in
the insulin dose or some noninsulin oral agents (i.e., sulfonylureas,
meglitinides) C. Decrease or delay in food intake
D. Increase in exercise levels
E. Alcohol ingestion (inhibits hepatic gluconeogenesis)
III. Prevention of hypoglycemia

A. Eat meals and snacks on time

B. Take insulin as directed at appropriate times
C. Make adjustments for decreased or delayed food intake
D. Take special care when sleeping late
1. May need to decrease the evening NPH dose by 10% to 15% if sleeping
more than 45 minutes later than usual 2. May require advancing the
entire day’s schedule
E. Make adjustments for increased activity or exercise
1. Avoid exercising alone
2. SMBG is essential: refer to Table 16-6 for specifics 3. If symptomatic
hypoglycemia occurs during exercise, stop and eat a snack
IV. Treatment of hypoglycemia (Table 16-11) V. Special problems related to hypoglycemia

A. Unawareness of hypoglycemia
1. Severe hypoglycemia without warning: patients with low A1c and
repeated episodes of recent hypoglycemia are most vulnerable 2.
Inability to recognize blood glucose levels <55 mg/dl: refer to an
endocrinologist
B. Dawn and predawn phenomena
1. Increase in blood glucose between 5 and 8 am (increased insulin
resistance because of cortisol and growth hormone surge) is known as
the dawn phenomenon
Table 16-11
Treatment of Hypoglycemia

582
 Type of
Symptoms Treatment
Hypoglycemia

Mild Hunger Give 10-15 g of simple carbohydrates*

Tremors and Should respond in 10-15 mins
palpitations
Sweating

Moderate As above plus: May require a second dose of simple carbohydrates

H/A The patient may have more difficulty treating hypoglycemia independently
Mood changes,
irritability
Drowsiness,
decreased
attentiveness

Severe Unresponsiveness No oral carbohydrate

Unconsciousness Glucagon 1 mg IM or SC in the deltoid or anterior thigh (0.5 mg if <5 yrs of
Convulsions age) Transfer to the ED after emergency treatment

*Each
of the following foods gives ∼10-15 g of carbohydrate:
• 4 oz (120 ml) fruit juice
• 8 Life Saver candies
• 1 tbsp honey or Karo syrup
• 2 tsp sugar or raisins
• 3 glucose tablets or gels Do not use chocolate, ice cream, or other fatty foods that delay glucose absorption and contribute to weight
gain.

2. Insulin requirements are generally at the lowest level in the predawn

period (1 to 3 am) 3. As a result of the previous two points, attempts to
normalize FBG levels can result in nocturnal hypoglycemia 4.
Identification and prevention
a) measure SMBG at hs, 2 to 4 am, and 7 am b) take bedtime snack
c) give the evening dose of NPH at hs
d) consider referral for an insulin pump with a variable programmable
basal rate

Hyperglycemia

I. Diabetic ketoacidosis (DKA)

A. Definition: characterized by metabolic acidosis, ketosis, and

hyperglycemia due to insulin deficiency B. Risk factors
1. Omission of insulin (type 1 or 2 DM)
2. New-onset DM, especially type 1 (20% to 25% of DKA cases)
3. Infection (30% to 40% of DKA cases)
4. Acute pancreatitis

583
 5. Acute MI or CVA
6. Medications (e.g., clozapine or olanzapine; cocaine; lithium)
C. Signs and symptoms: develops rapidly over 24 hours
1. Polyuria, polydipsia
2. Kussmaul’s respirations
3. Abdominal pain
4. Dehydration
5. May have a fruity odor to breath
6. Altered LOC
D. Lab values
1. pH <7.30
2. Glucose >500 to 800 mg/dl
3. Serum bicarbonate ≤15 mEq/L
E. Treatment: emergency transfer to ED; DKA is a medical emergency
II. Hyperosmolar hyperglycemic state (HHS)

A. Definition: severe hyperglycemia in the absence of ketosis

B. Risk factors
1. Inadequate insulin or noncompliance (21% to 41% of HHS cases)
2. Accompanying infection (32% to 60% HHS cases): pneumonia, UTI, or
sepsis 3. Acute illness
4. Type 2 DM (>35% are previously undiagnosed)
5. Older than 50 years of age
6. Diuretic therapy
7. Nursing home residents
C. Signs and symptoms: develops more insidiously
1. Polyuria, polydipsia
2. Weight loss
3. Significant dehydration

584
 4. Weakness
5. Hypotension
6. Altered LOC, possible coma
D. Lab values
1. pH >7.30
2. Glucose >600 mg/dl and often >1000 mg/dl
3. Serum bicarbonate >20 mEq/L
4. Osmolality >320 mOsm
E. Treatment: emergency transfer to ED; HHS is a medical emergency, with a
mortality rate of 12% to 42%

Sick day management guidelines for patients with type 1 diabetes

I. Monitoring

A. Check blood glucose levels q2-4h and check urine ketones with every
void, regardless of blood glucose levels B. The patient should call the
health care provider when preprandial blood glucose levels remain
>250 mg/dl or urine has moderate-to-large ketones
II. Insulin and diet

A. Do not stop insulin despite N/V or inability to eat (although the dose
may need to be temporarily adjusted to lower the risk of
hypoglycemia)
1. Usual dose of NPH or glargine or detemir insulin
2. For blood glucose levels >240 mg/dl, increase morning short-acting
insulin by 20%
3. For blood glucose levels >400 mg/dl, increase morning short-acting
insulin by 30%
4. If urine ketones are moderate to large, increase by an additional 10%
B. If no N/V and decreased activity (e.g., bed rest)
1. Decrease calorie intake by one third
2. Adjust insulin as mentioned above
C. If the patient is having N/V

585
 1. Use short-acting insulin only
2. Meal plan
a) sweetened liquids such as soft drinks, fruit juices, sweetened tea: 4 to 6
oz (120 to 180 ml) each hour for adults, 2 to 4 oz (60 to 120 ml) each
hour for children b) when tolerated, add soft carbohydrate foods
3. Some clinicians teach patients to replace usual carbohydrate calories
with “sick day” foods (Box 16-1)
III. Seek medical attention immediately when

A. Fever is >100°F
B. Diarrhea persists beyond 4 hours
C. The patient is vomiting and unable to take fluids for >2 to 4 hours D.
Blood glucose levels remain >250 mg/dl despite insulin adjustments
E. Moderate-to-large ketones appear in urine
F. The patient experiences severe abdominal pain or other unexplained
symptoms or has mental clouding G. Illness persists for >24 hours
Box 16-1

F o o d s A l l o we d o n S i c k D a y s

Choose one of these foods
for every fruit on your meal
plan (10 g of carbohydrate
each):
½ c regular ginger ale
½ c Kool-Aid
1 c Gatorade
½ c regular lemonade
1 Popsicle
½ c soft drink, 7-Up
¼ c regular gelatin
¼ c grape juice
⅓ c apple juice
¼ c cranberry juice
2 tsp syrup, sugar
Choose one of these foods for Choose one of these foods for
every milk product on your every starch product on your
meal plan (12 g of meal plan (15 g of
carbohydrate each): carbohydrate each):
½ c regular cocoa ½ c cooked cereal
¾ c cream soup ¼ c regular pudding
1 c whole milk ½ c ice cream
⅓ c tapioca pudding 1 c cream soup
¼ c vanilla pudding 1 c chicken noodle soup
¼ c custard ¼ c sherbet
1 tbsp sugar ⅓ c regular gelatin
Remember, you are taking sweetened 1 tbsp jelly
drinks and foods because you cannot ½ c instant breakfast
eat other foods!
5 vanilla wafers
6 saltine crackers
1 c milk

586
Chronic complications of DM

I. Retinopathy

A. Leading cause of impaired vision in adults aged 25 to 74 years; much

of the visual loss can be prevented by timely identification and
treatment
1. Type 1: begins 3 to 5 years after diagnosis and almost all patients have
it after 15 to 20 years 2. Type 2: 50% to 80% patients have it 20 years
after diagnosis
B. Screening/evaluation: yearly dilated eye examination with an
ophthalmologist or optometrist
1. All patients with type 1 DM of ≥5 years’ duration
2. All type 2 DM patients
3. Early in the first trimester for any pregnant woman with known DM
C. Treatment
1. Usually laser surgery
2. Optimal glycemic control reduces incidence and progression
II. Nephropathy

A. Leading cause of end-stage renal disease; 20+ years after DM

diagnosed, reported in 30% to 40% of patients with type 1 DM and
15% to 20% of patients with type 2 DM
B. Screening/evaluation (do not use diagnosis of DM nephropathy
without protein in urine)
1. Yearly urine for albuminuria (albumin-to-creatinine ratio [ACR]) 2. If
positive, repeat the test twice in a 3-to 6-month period; if two or three
tests are positive for severely increased albuminuria, begin treatment
a) microalbuminuria: moderately increased, 30 to 300 mg/g
b) macroalbuminuria: severely increased, >300 mg/g
3. Sudden decrease in insulin requirements can indicate renal
compromise
C. Treatment
1. At the time of initial diagnosis, R/O other causes of renal disease (e.g.,

587
 obstructive uropathy, infection) 2. Aggressive glycemic control
3. For treatment of macroalbuminuria, begin ACE or ARB at usual doses
(see Table 8-15); HTN does not need to be present 4. Aggressively
monitor and treat HTN
5. Treat hyperlipidemia (see Chapter 8, Hyperlipidemia) 6. Consider
referral to a nephrologist or DM specialist with serum creatinine >2
mg/dl, eGFR <45 ml/min, or ACR >300 mg/g 7. Promptly treat UTIs;
repeat UA after treatment
III. Neuropathy

A. Types
1. Peripheral
a) insidious onset, symmetric distribution, progressive course
b) may affect cranial or peripheral nerves (often in the feet first) c) may
present as nerve or skin pain, paresthesias, or muscle pain
2. Autonomic
a) GI: may have GERD, gastroparesis (consider with early satiety, N/V,
bloating, and postprandial abdominal fullness), diarrhea, constipation,
or incontinence b) GU: may have neurogenic bladder, sexual
dysfunction
c) CV: may have tachycardia, exercise intolerance, orthostatic
hypotension
B. Screening/evaluation
1. Yearly examinations for sensation using a monofilament (see Figure
16-1) 2. EMG, if indicated
3. Ankle-brachial index: obtain if experiencing claudication or with a
venous filling time of >20 seconds; to evaluate venous filling time
a) with the patient supine, identify a prominent pedal vein; elevate the
leg to 45 degrees for 1 minute until the vein collapses b) have the
patient sit up with the leg hanging over the examination table and note
the time until the pedal vein bulges
4. Assess skin integrity of feet, especially between toes and under
metatarsal heads, at least annually; note the presence of redness,
increased warmth, or callus formation 5. R/O conditions that may

588
 mimic diabetic neuropathy: heavy ETOH use, uremia, pernicious
anemia, and exposure to chemical toxins
C. Treatment
1. Optimal glycemic control
2. Foot care (see Foot Care Instructions, later in this chapter) 3.
Pain/paresthesias: one or more of the following may help:
a) antidepressants
(1) nortriptyline 10 to 25 mg hs; increase the dose q2wks to 75 mg or until
the dose is not tolerated (not to be used in patients with cardiac
disease) (2) duloxetine 20 to 60 mg hs
b) anticonvulsants
(1) pregabalin 50 mg bid, slowly increase to 300 mg qd total (150 mg bid
or 100 mg tid) (2) gabapentin 300 to 1800 mg qd in three divided doses
c) others
(1) alpha-lipoic acid (ALA) 600 mg once qd may help
(2) Metanx 1 cap bid
4. Muscle pain
a) NSAIDs
(1) avoid with eGFR ≤60 ml/min
(2) use cautiously with eGFR 60 to 89 ml/min plus other conditions such
as HF, cirrhosis, or diuretic use
b) physical therapy
c) muscle relaxants
d) avoid alcohol (may aggravate the development of neuropathy)
5. GI problems
a) small, frequent meals
b) avoid fats
c) refer to a GI doctor with continued symptoms
IV. DM foot ulcer

A. Results from decreased sensation and microvascular circulation;

589
 neuropathy is a contributing factor because injury is not found until
damage has occurred B. Description
1. Painless ulcers usually noted on the plantar surface of the foot
(commonly over metatarsal heads, heels, or sites of poorly fitting
shoes)
a) grade 1: superficial, involving full skin thickness but not underlying
tissues b) grade 2: deep, penetrating down to the ligaments/muscle,
but no bone involvement or abscess c) grade 3: deep, with cellulitis or
abscess formation; often with osteomyelitis d) grade 4: localized
gangrene
e) grade 5: extensive gangrene of the entire foot
2. Feet may be warm or cool to touch; usually diminished pedal pulses 3.
Paresthesias in part or all of the affected extremity
C. Treatment
1. Aggressive control of DM
2. If the vascular status of the limb is compromised, refer to a vascular
surgeon 3. Grade 1 and 2
a) extensive debridement, good local wound care, and relief of pressure
on the ulcer b) if infection is present (obvious purulent drainage or
redness/swelling or warmth around the ulcer): culture ulcer base after
debridement and treat according to C&S
c) if the ulcer is not improving after 3 to 4 weeks of above therapy, refer
to a wound specialist or surgeon
4. Grade 3: refer to a surgeon or wound care specialist after obtaining
ABI and bilateral venous Doppler (to check circulation) and bone scan
(to check for osteomyelitis) 5. Grade 4 and 5: urgent referral to ED for
hospital admission and treatment

Foot care instructions for people with diabetes

I. These guidelines assume that the person has risk factors for foot problems: neuropathy,
vascular disease, or a combination of these. They are meant to be used as patient teaching points.
II. Footwear

A. Wear shoes that fit properly: look for a wide toe box rather than
pointed toes, avoid high heels, leather or canvas shoes are best, and

590
 buy shoes at the end of the day (when your feet are larger) for the best
fit B. Change your shoes once or twice during the day to relieve areas
of pressure
C. Never go barefoot, even at home; especially, avoid walking on hot
concrete or sand D. Avoid thongs, sandals, or open-toed shoes
E. Break shoes in slowly; wear them for only a few hours a day at first,
then gradually build up the wearing time F. Before wearing shoes,
always check the insides for nail points, worn areas, foreign objects, or
other rough areas that might cause blisters or rubbing G. Wear
appropriate shoes for the weather; avoid wearing wet shoes
III. Foot care

A. Check your feet (tops, bottoms, sides, between toes) daily for blisters,
cuts, scratches, changes in color or discoloration, or changes in
temperature; use a mirror if necessary or have someone check your
feet for you B. Wash feet daily with mild soap and warm (not hot)
water; dry thoroughly and carefully, especially between toes C. Use
creams or petroleum jelly to moisturize skin daily; do not place creams
or lotions between toes D. Wear clean socks daily; be sure that the
socks are appropriate for the type of shoes worn; do not wear darned
or mended socks or socks with holes and avoid socks with seams E.
Avoid soaking feet
F. Avoid temperature extremes: check water temperature with your
elbow before putting your feet in G. Avoid all OTC treatments for
corns, calluses, and nails; do not use strong antiseptics, astringents, or
alcohol on your feet H. Trim nails “to the shape of the end of your toe”
(i.e., straight across with slightly rounded edges); do not cut into the
corners I. No “bathroom surgery”: do not cut corns and calluses
yourself, as these should be managed by an experienced health care
provider J. Avoid using adhesive tape on your feet
K. Wear socks if your feet are cold; do not put heating pads or hot water
bottles on your feet L. Avoid garters, tight elastic bands on socks, or
anything that decreases circulation to your feet (including crossing
your legs) M. Contact your health care provider when you
1. Notice cuts, blisters, or breaks in the skin of your feet
2. Have ingrown nails

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3. Notice changes in the color of your feet
4. Have pain or changes in the sensation in your feet
5. Notice a change in the shape or architecture of your foot
N. Other things you can do to prevent foot problems
1. Stop smoking
2. Control your weight, BP, and blood glucose
3. Get regular exercise
4. Have your health care provider check your feet at each visit
5. Orthotics or diabetic shoes may be necessary, especially if there are
skin changes, calluses, or foot shape changes

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CHAPTER 17

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Pediatric conditions
For details regarding complete history and physical examination, see Chapter 2.

Fever in infants and children

I. Description

A. Fever is any body temperature >99°F; it is a therapeutic response by

the body’s immune system to try to rid itself of detrimental bacteria or
virus
1. Evaluate fever if
a) present in neonates or infants aged <3 months
b) persisting >4 to 5 days or sudden elevation in temperature >102°F
c) development of new localized symptoms
d) persistent fever in the presence of underlying medical problems (e.g.,
heart disease, lung disease, immunocompromised, cancer)
2. With fever <102°F, lasting >4 to 5 days along with any of the following
symptoms, evaluate further
a) flushing
b) restlessness, inconsolable crying
c) anorexia
d) tachycardia, seizure, tachypnea
e) lethargy
3. If the child has febrile seizures
a) may occur with sudden rise or fall in temperature, but many times
there is no known cause b) there is no evidence that a decrease in
fever, by any means, will stop or prevent febrile seizures c) most
common between the ages of 6 months and 5 years
d) all infants should be evaluated when febrile seizures occur
e) febrile seizure does not mean that the child has a seizure disorder

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II. Causes of fevers

A. Any infection (e.g., pneumonia, strep throat, appendicitis)

B. May see low-grade fever after immunizations (usually <102°F)
C. Teething
D. Viral infection
E. Cancer
III. Diagnostic testing

A. CBC
1. Elevated WBCs with increased neutrophils: bacterial infection
2. Decreased WBCs with increased lymphocytes: viral infection, pertussis
3. Greatly elevated WBCs with lymphadenopathy: suspect leukemia or
lymphoma
B. ESR elevated with negative RF, ANA: suspect malignancy
C. Urinalysis positive for leukocyte esterase, nitrite, and bacteria: obtain
urine culture D. Influenza
E. Rapid strep
IV. Treatment

A. Nonpharmacologic treatment
1. Fever <102.2°F should only be treated if the child is uncomfortable or
could become dehydrated 2. If fever is mild and the child seems
unaffected, do not give antipyretics; the goal is to lower, not eliminate
fever; keep the child quiet and resting 3. Keep the child well hydrated
(see Table 10-5 for oral rehydration solution) and monitor for
dehydration (see Table 17-1)
4. Keep the environment comfortable and do not “bundle up” the infant
or child; remove any excess clothing and use a lightweight sheet to
cover the child 5. Tepid sponge baths with both the parent and the
child sitting in a tub (caution the parent not to leave the infant or child
alone in the bath)
B. Pharmacologic treatment
1. Identify and manage the cause of fever

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 2. Give antipyretics to reduce temperature (see Tables 17-2 and 17-3)
a) antipyretics can be alternated if fever is not under control with one
product within 4 hours b) DO NOT give acetaminophen and ibuprofen
together, this increases the chances of overdosing the child c)
acetaminophen dose: 10 to 15 mg/kg q4-6h; not to exceed 5 doses in 24
hours (see Table 17-2 for dosing) d) ibuprofen 100 mg/5 ml dose:
10mg/kg q6-8h: not to exceed 40 mg/kg/24 h (see Table 17-3 for dosing)
e) aspirin is not the drug of choice because of association with Reye’s
syndrome, bleeding disorders, and hypersensitivity
3. Antipyretic medication precautions
a) acetaminophen
(1) monitor liver function if the child is taking barbiturates,
carbamazepine, isoniazid, rifampin, or sulfinpyrazone (2) some
acetaminophen preparations contain aspartame; infants and children
with phenylketonuria should not take these preparations
b) ibuprofen
(1) give with food and monitor for gastritis
(2) do not give to infants aged <6 months because of increased potential
for renal impairment
C. Refer
1. Infants aged < 3 months
2. Fever >104°F and unable to lower fever
3. The child appears ill, drowsy, or nonresponsive or has a seizure
Table 17-1
Clinical Signs and Treatment of Dehydration in Children

Type of
Mild Moderate Severe
Sign
Activity/mental Normal Lethargic, irritable, restless Listlessness to coma state
status

Color Pale Pale-grayish Mottled and cool

extremities, cyanosis

Eyes Normal, tears present Diminished or no tear production Deeply sunken with tears
absent

Thirst Normal to slightly Moderately increased Very thirsty but may be

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 increased too lethargic to take
liquids

Urine output Decreased (<1-2 Oliguric (1 diaper qd or <1 ml/kg/h) Anuria

diapers qd or <2-3 Specific gravity >1.030 Specific gravity >1.030
ml/kg/h)

Fontanelle Flat Slightly depressed Sunken fontanelle and

eyes

Mucous Slightly dry lips with Very dry lips and oral mucosa with very little Cracked lips and dry oral
membrane decreased, thickened saliva mucosa
saliva

Skin turgor and Slight decrease Marked decrease Tenting

elasticity

Pulse Normal to slightly Increased Tachycardic at rest but

increased may become bradycardic
as dehydration worsens

Capillary refill <1.5 sec 1.5-3 sec >3 sec

Blood pressure Normal Normal to slightly decreased Decreased

Weight loss 5% 10% 15%

Treatment Rehydrate at 10 ml/kg Be aggressive with rehydration; if infant or child Emergent transfer to ED,
of appropriate will not or cannot cooperate or tolerate fluids, may need to call for
formula, liquids, or transfer to the nearest hospital for IV fluids ambulance
foods Initiate IV fluids if
Replace each fluid loss possible
or give 1-2 tbsp of Start O2 while awaiting
fluids q30min
transportation
Avoid fluids and foods
high in fat, simple
sugars, and whole milk

Table 17-2
Acetaminophen Fever Control Chart

Chewable Junior Strength Chewable Tablets Elixir 1 tsp = 160

Age Weight *
Tablet (80 mg) and Caplets (160 mg) mg/5 ml
0-3 6-11 lb (2-5 N/A N/A ¼ teaspoon (1.25
mos kg) ml=40 mg)
4-11 12-17 lb (6- N/A N/A ½ teaspoon (2.5
mos 7 kg) ml=80 mg)
12-23 18-23 lb (8- 1.5 tab (120 mg) N/A ¾ teaspoon (3.75
mos 10 kg) ml=120 mg)
2-3 24-35 lb 2 tab (160 mg) 1 tab 1 teaspoon (5
yrs (11-15 kg) ml=160 mg)
4-5 36-47 lb 3 tab (240 mg) 1.5 tab 1½ teaspoon (7.5
yrs (16-21 kg) ml=240 mg)
6-8 48-59 lb 4 tab (320 mg) 2 cap or tab (320 mg) 2 teaspoon (10
yrs (22-26 kg) ml=320 mg)

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 9-10 60-71 lb 5 tab (400 mg) 2½ cap or tab (400 mg) 2½ teaspoon (12.5
yrs (27-32 kg) ml=400 mg)
11-12 72-95 lb 6 tab (480 mg) 3 cap or tab (480 mg) 3 teaspoons (15
yrs (32-43 kg) ml=480 mg)
>12 96+ lb Can use adult dosing schedule
yrs
*Dosage
should be calculated by weight and not age. Ensure that the caregiver has an accurate measuring device.

Table 17-3
Ibuprofen dosing chart

Infant Drops Children’s Liquid Chewable Junior strength

Age* Weight† (50 mg/.1.25 1 tsp = 100 mg/5 Tablet 1 tab = Tablets 1 tab = 100
ml) mL 100 mg mg
6-11 12-17 lb 1.25 ml (50 0.5 ml (50 mg) N/A N/A
mos (5.4-8.1 mg)
kg)
12-23 18-23 lb ¼ teaspoon ¾ teaspoon N/A N/A
mos (8.2-10.8 (1.8 ml=75 mg) (3.75ml=75 mg)
kg)
2-3 yrs 24-35 lb 1 teaspoon (5 1 tab N/A
(10-16.3 ml=100 mg)
kg)
4-5 yrs 36-47 lb N/A 1½ teaspoons (7.5 1½ tab N/A
(16.4-21.7 ml=150 mg)
kg
6-8 yrs 48-59 lb N/A 2 teaspoons (10 2 tab 2 tab (200 mg)
(21.8-27.2 ml=200 mg)
kg)
9-10 yrs 60-71 lb N/A 2½ teaspoons (12.5 2½ tab 2 tab (250 mg)
(27.3-32.6 ml=250 mg)
kg)
11 yrs 72-95 lb N/A 3 teaspoons (15 3 tab 3 tab (300 mg)
(32.7-43.2 ml=300 mg)
kg)
>12 yrs
Use
adult
dosing
*
Do not give to infants aged <6 months.
†
Dosage should be based on weight. Ensure that the caregiver has an accurate measuring device.

Failure to thrive (FTT)

I. Description

A. Children aged <2 years who fail to gain weight, fall below the 5th

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 percentile on growth charts, or drop more than 2 SD on the growth
curve without an obvious organic etiology are defined as having a
nonorganic failure to thrive B. This occurs at an important time of
growth and development; poor nutrition can delay mental
development
II. History: inquire about the following:

A. Organic illness (e.g., cleft palate, CF, protein allergy, growth hormone
deficiency, chronic infections) B. Bonding with the parent or caregiver
C. Detailed feeding and dietary history, including amounts of
formula/breast feeding and patient satisfaction after eating
III. Signs and symptoms of undernourishment

A. Disinterest in surroundings; avoidance of eye contact or poor

socialization with peers B. Irritability
C. Delays in growth and development and inability to reach normal
milestones (see Table 2-1)
IV. Diagnostic testing (see Chapter 4): CBC, urinalysis, CMP
V. Treatment

A. Speech therapy consultation for swallowing dysfunction

B. Dietician consultation
C. Closely monitor weekly weights
D. Encourage more high-calorie frequent feedings and for toddlers,
encourage more high-protein snacks in between meals E. Referral to a
pediatrician if unable to gain weight or developmentally delayed

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Upper respiratory tract disorders
Acute otitis media (AOM)

I. Description: inflammation or infection (e.g., bacterial or viral) of the middle ear with purulent
effusion II. Bacterial/viral causes

A. Streptococcus pneumoniae, Haemophilus influenzae, M. catarrhalis

B. RSV, adenovirus, influenza
III. Environmental causes

A. Exposure to other sick children (i.e., daycare, school, or siblings)

B. Passive exposure to smoke
C. Sleeping with a bottle
IV. Signs and symptoms

A. Non-severe illness: mild otalgia or fever <102°F in the past 24 hours;

the preverbal child may pull at ears or hair near the ear to signify pain
B. Severe illness: moderate-to-severe otalgia or fever ≥102°F in the past
24 hours; the child may cry inconsolably and have otorrhea if TM has
perforated C. TM will be abnormal in color (e.g., reddish to
hemorrhagic) with moderate to severe bulging, impaired mobility and
possible perforation
D. Fever
E. H/A, sinus congestion, and rhinorrhea
F. Hearing loss or decreased hearing in the affected ear
V. Diagnostic testing: pneumatic otoscopy (e.g., tympanometer) for mobility
VI. Treatment

A. Conservative treatment for acute AOM with pain management if the

child is >2 years old, TM is intact, fever is <102°F, and the child does
not appear ill
1. Use acetaminophen or ibuprofen (see Tables 17-2 and 17-3) and 2. Can
use topical analgesic drops (e.g., antipyrine/benzocaine [Auralgan]) if
no perforation is noted
B. Closely follow-up with the parent to monitor pain and overall
symptoms; if no improvement in 48 to 72 hours, start antibiotics

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 (typically AOM will resolve or improve within 24 to 48 hours) C.
Antibiotics should be used for severe AOM in patients aged 3 months
to 2 years in the following cases:
1. The child appears ill with unilateral or bilateral AOM
2. Fever is >102°F with severe otalgia or otorrhea for >48 hours
D. Antibiotic treatment is for 10 days (can treat for 5 to 10 days if first
time and non-severe AOM)
1. Amoxicillin <2 months of age: 30 mg/kg/day ÷ q12h; 2 months to 12 years:
80 to 90 mg/kg/day ÷ q12h 2. Amoxicillin/clavulanate (Augmentin) <3
months of age: 30 mg/kg/day ÷ q12h; >3 months of age, <40 kg: 25 to 45
mg/kg/day ÷ q12h; >40 kg: use adult dosing 3. Cefuroxime (Ceftin) 2
months to 12 years: 30 mg/kg/day ÷ q12h
4. Azithromycin >6 months of age: 10 mg/kg qd for 3 days
E. Follow-up in 48 to 72 hours; if symptoms have not improved, consider
treatment failure and switch antibiotics and continue for 10 days
1. Clarithromycin 2 months to 12 years: 15 mg/kg/day ÷ q12h
2. Cefdinir 2 months to 12 years: 14 mg/kg/day ÷ q12h or q24h
3. Ceftriaxone 50 mg/kg IM daily for 1 to 3 days (can be used with failure
of PCN) 4. Clindamycin 2 months to 12 years: 30 to 40 mg/kg/day ÷ q8h
F. Refer to a pediatric ENT specialist if unresolved and/or aged < 2
months

AOM complicated by perforated TM

I. Usually heals within 4 to 6 weeks

II. Treatment

A. Amoxicillin 2 months to 12 years 80 to 90 mg/kg/day ÷ q8h for 10 days

B. If penicillin allergy, azithromycin 2 months to 12 years: 10 mg/kg on
day 1, then 5 mg/kg on days 2 to 4
C. Ciprofloxacin/dexamethasone otic >2 months of age: 4 gtts bid for 10 to
14 days D. Keep all water out of the ear until TM heals using a cotton
ball saturated with petrolatum before hair washing; no swimming or
other water exposure until healed; do not use ear plugs or try to clean
out the ear with a Q-tip E. Refer to an audiologist or ENT with any

601
 concern about hearing loss or recurrent perforation

AOM with tympanostomy tubes (TT)

I. Treatment: may need to clear debris out of ears and place ear wicks

A. Ciprofloxacin/dexamethasone otic >6 months of age: 4 gtts bid for 7

days B. Ofloxacin otic for 10-14 days, >6 months of age: 5 gtts bid; >13
years of age: 10 gtts bid C. No water exposure while under treatment
and until perforation has healed. Use a cotton ball saturated with
petrolatum and gently insert into the outer auricular opening while
showering/hair washing.
D. Do not use analgesic eardrops with TT or with perforation
E. Can use acetaminophen or ibuprofen orally (see Tables 17-2 and 17-3)
for discomfort F. Follow-up in 2 weeks or sooner if not resolving
II. Refer for persistent AOM (with perforation or TT) that does not respond to treatment

Otitis media with effusion (OME)

I. Description: middle ear effusion without acute signs of infection that usually occurs after AOM
as an inflammatory response or with eustachian tube obstruction II. Signs and symptoms

A. Decreased hearing, hearing loss, and fullness in ears

B. Opaque and retracted TM with limited mobility
C. Observable air-fluid levels
III. Diagnostic testing: usually tympanometry and pneumatic otoscopy
IV. Treatment

A. Early ID and referral to ENT with potential risk for hearing, speech, or
learning disability B. Monitor children with a low risk by “watchful
waiting” for 3 months from the onset of effusion C. Reevaluate with
persistent OME (with low risk) q3-6mo or until effusion resolves. If
hearing deficit is noted or structural abnormalities are suspected (e.g.,
cholesteatoma, perforation), refer to ENT.
D. Autoinflation may accelerate recovery; have the child chew gum,
blow up balloons, or puff cheeks out and swallow E. Avoid exposure
to smoking
F. Maintain immunizations, especially pneumococcal vaccine, in children
>2 years of age G. Antibiotics, steroids, antihistamines, or

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 decongestants have not been shown to improve outcomes

Otitis externa (swimmer’s ear)

I. Description: inflammation of the EAC or auricle

II. Causes: increased moisture (which disrupts normal flora of the canal) due to swimming in
fresh or chlorinated water, high environmental temperatures, chronic use of ear plugs or hearing
aids, and removal of packed cerumen with trauma to the canal III. Signs and symptoms

A. Discomfort limited to the EAC but may involve the entire ear
B. Redness of the EAC and swelling that may completely occlude the ear
canal
C. Discharge from the ear (otorrhea)
IV. Treatment

A. Removal of debris either with suction (if available) or gentle removal

with a Q-tip; can instill an ear wick to try to remove thin secretions B.
Discourage use of an ear spoon or curette because of trauma; do not
flush the canal unless TM is visualized (in case of perforation) C. Use
an ear wick for topical antibiotic therapy, especially if the secretions
cannot be removed D. Topical antibiotic therapy (drops can be instilled
over ear wicks)
1. Ofloxacin otic (Floxin Otic) >6 months of age: 5 gtts qd for 7 days 2.
Ciprofloxacin/dexamethasone (Ciprodex) >6 months of age: 4 gtts bid
for 7 days 3. CiproHC otic >1 year of age: 3 gtts q12h for 7 days (use
with intact TM only) 4. Neomycin/polymyxin/hydrocortisone otic
(Cortisporin otic) >2 year of age: 3 gtts 3 to 4 times qd for 10 days (use
with intact TM only)
E. Pain control is usually accomplished with NSAIDs and/or
acetaminophen (see Tables 17-2 and 17-3) F. Refer to ENT for
persistent symptoms, if deeper tissue infection is noted or if the patient
is immunocompromised or at higher risk for malignant external otitis
V. Prevention

A. If involved in water sports, use earplugs, shake water from ears, or

use blow dryer to ears after water exposure (safe distance is
considered about 12 inches from ear) B. After each water exposure,
mix rubbing alcohol and vinegar in 1:1 ratio and instill a few drops in
both ears C. Hearing aids (if used) should be removed each night and

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 cleaned according to the manufacturer’s directions D. Discourage
cleaning ears with “anything smaller than the elbow”

Allergic rhinitis

I. Description: an IgE-mediated allergic response to substances that have been inhaled; can be
seasonal or perennial; most common offenders are pollens, grasses, trees, and animal dander II.
Signs and symptoms

A. Red, itchy, and watery eyes; occasional periorbital swelling; dark

circles under eyes (“allergic shiners”) B. Stuffy, runny nose (clear
rhinorrhea), sneezing, H/A
C. Blue to pink boggy nasal turbinates with white exudate
D. Allergic “salute,” and persistent “gaping mouth”
E. Mouth breathing and snoring; dry cough
F. Sore throat with lymphoid hyperplasia of the posterior pharynx
III. Diagnostic testing: nasal swabs or CBC for eosinophils
IV. Treatment: Involves distancing from the allergen if possible plus

A. Decongestant of choice or
B. OTC antihistamine: one of the following either routinely or prn or
1. Hydroxyzine 2 to 4 mg/kg qd q6h
2. Loratadine 2.5 to 10 mg qd; for age >2 years
3. Cetirizine (Zyrtec) 2.5 to 10 mg qd; for age >2 years
4. Fexofenadine (Allegra) 30 mg bid for age >6 years
5. Desloratadine (Clarinex) 5 mg qd for age >12 years
C. Leukotriene antagonist: Montelukast (Singulair) 4 or 5 mg qd hs
depending on age D. Intranasal steroids (use in each nostril)
1. Beclomethasone (Beconase AQ) 6 to 12 years of age: 1 to 2 sprays bid 2.
Mometasone furoate (Nasonex) 2 to 12 years of age: 1 spray qd; >12
years: 2 sprays qd 3. Fluticasone (Flonase) for children >4 years of age: 1
spray qd
E. Cromolyn sodium 1 spray each nostril q4h (onset takes ∼2 to 4
weeks); not a steroid; start before known exposure F. Ophthalmic mast
cell stabilizers

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 1. Olopatadine ophthalmic (Patanol) or azelastine (Optivar) >3 years of
age: 1 gtt in eye(s) bid 2. Ketotifen (Zaditor) >3 years of age: 1 gtt in
eye(s) q8-12h
G. Follow-up
1. Monitor for hearing decrease or loss with long-term chronic allergic
rhinitis 2. Nosebleeds may be caused by lack of humidity in the
environment or chronic use of nasal steroids 3. If the child is >16 years
of age, may consider annual IM steroid at the lowest effective dose 4.
Evaluate the environment for dust and mold, do not let pets sleep with
the child, remove carpets, use allergen-proof pillow covers, and wash
bed linens weekly
H. Referral to an allergist if symptoms become unmanageable

Common cold

I. Description: an acute, self-limited viral illness involving the upper respiratory tract II. Signs
and symptoms

A. In infants: may see nasal discharge and fever with increased fussiness,
decreased appetite, and difficulty sleeping B. In school-age children:
may have nasal congestion, runny nose, cough, and sneezing with
occasional low-grade fever and H/A
III. Treatment is conservative and symptoms should resolve within 10 days

A. Humidifier, increase oral intake

B. Analgesics for pain/discomfort and rest (see Tables 17-2 and 17-3) C. If
symptoms persist >10 days without improving, may consider possible
secondary infection

Acute bacterial rhinosinusitis

I. Description: a secondary bacterial infection occurring in one or more of the paranasal sinuses;
usually occurs after viral illness and is a common problem in children
II. Signs and symptoms

A. Persistent purulent nasal discharge and/or cough for >10 days with no
improvement B. May have a fever >102.2°F for >3 days or new onset of
fever >5 days after the illness started C. Initial symptoms improve but
then worsen or new onset of fever and/or H/A
D. Not to be missed

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 1. Redness and swelling of eyelids and periorbital area and no proptosis
or pain with EOM: consider periorbital cellulitis 2. Pain with eye
movement, conjunctival swelling, periorbital swelling, and erythema
with H/A: consider orbital cellulitis 3. Fever, H/A, nuchal rigidity,
confusion/lethargy: consider meningitis
4. Headache, fever and change in the mental status, drowsiness, muscle
weakness: consider brain abscess
III. Treatment for symptom control

A. Normal or hypertonic saline nasal spray/irrigation frequently (e.g., 8

to 10 times qd) (see Chapter 7, Practice Pearls for ENT) B. Analgesics
for pain (see Tables 17-2 and 17-3) C. Humidifier in the room and
warm steamy showers 2 to 3 times qd
D. Antibiotic treatment for 10 days
1. Amoxicillin/clavulanate <3 months of age: 30 mg/kg/day ÷ q12h; >3
months of age: <40 kg : 25 to 45 mg/kg/day ÷ q12h; >40 kg : use adult
dosing 2. Amoxicillin <2 months of age: 30 mg/kg/day ÷ q12h; 2 months
to 12 years of age: 80 to 90 mg/kg/day ÷ q12h 3. Cefdinir 2 months to 12
years of age: 14 mg/kg/day ÷ q12h or q24h
4. Cefpodoxime 2 months to 12 years of age: 10 mg/kg/day ÷ q12h

Pharyngitis

I. Description: inflammation of the pharynx; most commonly caused by group A β-hemolytic

streptococcus or viral infection II. Bacterial signs and symptoms

A. Moderately ill appearing patient with a complaint of sore throat

B. Tonsillar exudate, tender anterior cervical lymphadenopathy, fever,
and absence of cough
1. If all the above four symptoms are present, treat as a bacterial infection
with antibiotics before culture (culture should be done for all children
aged <16 years) 2. If two or three of the above symptoms are present,
culture first and if positive, then treat with antibiotics 3. If one or none
of the above symptoms are present, it is probably viral and no
antibiotics are recommended
C. May have scarlatina rash (fine sandpaper feel) that presents as a
blanchable red rash on the face and torso (see Color Plate 14) D.

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 Petechial appearance on the soft palate; a bright red tongue with white
coating (strawberry tongue)
III. Viral signs and symptoms (usually last 3 to 7 days)

A. Mildly to moderately ill; low-grade fever

B. Conjunctivitis, coryza and cough, hoarseness
C. Preauricular lymphadenopathy
D. Sore throat, mouth or lip ulcers
IV. Diagnostic testing

A. Rapid strep test; if negative, consider throat culture

B. Consider CBC for leukocytosis; if negative, consider monospot test
V. Antibiotic treatment

A. Bacterial pharyngitis: antibiotics given orally for 10 days, except as

noted
1. Amoxicillin <2 months of age: 30 mg/kg/day ÷ q12h; 2 months to 12 years:
80 to 90 mg/kg/day ÷ q12h 2. Cephalexin >1 year of age: 40 mg/kg/day ÷
q12h
3. Cefdinir 6 months to 12 years: 14 mg/kg/day ÷ q12h
4. Azithromycin >2 years of age: 12 mg/kg/day for 5 days
5. Penicillin G 1.2 million U IM once in patients >27 kg; 600,000 U IM
once in patients <27 kg
B. Follow-up in 48 hours if bacterial infection; if symptoms are not
improving, consider switching to
1. Clindamycin 7 mg/kg q8h for 10 days
2. Amoxicillin/clavulanate <3 months of age: 30 mg/kg/day ÷ q12h; >3
months of age, <40 kg : 25 to 45 mg/kg/day ÷ q12h; > 40 kg : use adult
dosing
VI. Symptomatic treatment for pharyngitis

A. Saltwater gargles, soft and cool foods, throat lozenges, rest, and
increased fluids B. Analgesics for pain or fever (see Tables 17-2 and 17-
3) C. No sharing utensils or drinks, encourage covering mouth when
coughing, decrease mouth to mouth contact D. Discard toothbrush
immediately and buy two new toothbrushes; use one for 48 hours,

607
 then discard E. Child with strep pharyngitis can return to school after
antibiotic therapy for 24 hours and/or when fever resolves

Influenza

I. Description: a very contagious viral illness that occurs suddenly and causes URI symptoms;
easily spreads through schools, daycares if individuals are not immunized against flu; spreads
by droplets from coughing, sneezing, and hand contact with the infected individual II. Signs and
symptoms

A. Sudden high fever (can be >102.2°F), myalgia, cough, sore throat,

watery runny nose B. The patient may become dehydrated, have
tachypnea, tachycardia, facial pain, and H/A C. Occasionally will have
N/V/D
III. Diagnostic testing: antigen detection testing from nasopharyngeal surface for Flu A & B
IV. Pharmacological treatment for 5 days; best if started within 48 hours of symptoms

A. Oseltamivir (Tamiflu) bid

1. 2 weeks to 11 months: 3 mg/kg
2. Older than 1 year or <15 kg: 30 mg
3. Older than 1 year or 15 to 23 kg: 45 mg
4. 23 to 40 kg: 60 mg
5. Greater than 40 kg: 75 mg
B. Zanamivir 10 mg (Relenza) two inhalations bid for 5 days for infected
patients aged >7 years and prophylaxis for patients aged >5 years
(adult and pediatric dosing is same) C. Prophylactic treatment with
zanamivir (Relenza) or oseltamivir (Tamiflu): duration is 7 days if
exposure is outside the house; 10 days if household exposure; 14 days
in institutionalized settings (start prophylaxis at onset of identified flu
outbreak add)

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Lower respiratory tract disorders
Croup

I. Description: a viral illness that affects the larynx and trachea (may extend to the bronchi) of
children; usually occurs during fall and early winter II. Signs and symptoms

A. Usually illness begins as a URI infection with low-grade fever but

within 1 to 2 days, the child has hoarseness, barky cough, and stridor
B. The hallmark sign is stridor: harsh, high-pitched sound produced by
a partially obstructed upper airway C. Mild croup
1. Barky cough
2. No audible stridor at rest but has stridor if active
3. None or very mild intercostal retractions
D. Moderate croup
1. Stridor with rest, mild retractions, and little or no agitation
2. Decreased air entry and cyanosis
3. The child does not appear toxic
E. Severe croup
1. Significant stridor at rest (stridor that “improves” may be a sign of
worsening obstruction) 2. Decreased airway entry, cyanosis, intercostal
retractions with in-drawing of the sternum 3. Anxious, agitated, or
fatigued
4. Respiratory symptoms typically worsen at night; resolve within 3 to 7
days
III. Diagnostic testing if not acutely ill

A. Lateral neck x-ray to check for “steeple sign” of epiglottis

B. CXR usually shows hyperinflation and mild infiltrates
IV. Treatment

A. Treatment for mild-to-moderate croup in office

1. Nebulized racemic epinephrine 1:1000 solution diluted in 3 ml normal
saline or premixed tubule of 0.5 ml once, followed by: 2. Oral
dexamethasone 0.15 mg to 0.6 mg/kg (maximum dose 10 mg) in a

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 cherry-flavored syrup as a single dose (the IV/IM preparation [4
mg/ml] can be given mixed in syrup at 0.6 mg/kg) or 3. Dexamethasone
0.6 mg/kg IV/IM once or
4. Prednisolone (Prelone, Pediapred) 1 to 2 mg/kg/day PO in a single qd
dose for 3 to 5 days or 5. Nebulized budesonide (Pulmicort) 0.25
mg/2ml bid (not as effective for immediate results) for 3 to 5 days 6.
Cool mist humidifier near face
7. Discharge criteria for mild croup after office treatment: return of a
more normal respiratory rate and normal pulse ox, with no dyspnea
a) no stridor at rest
b) can tolerate fluids by mouth
c) improved behaviors
d) can usually go home safely
8. Home care should include the following:
a) instruction to parents to go to ED if symptoms recur or get worse
b) analgesics routinely for discomfort (see Tables 17-2 and 17-3) c) cool
mist humidifier near face; if stridor recurs, immediately go to the
bathroom and turn on hot water and sit with the child in a steamy
room until symptoms improve; if symptoms do not improve, go to ED
d) rest and try to keep the child quiet
e) oral fluids to prevent dehydration (see Table 10-5 for oral rehydration
solution) f) nebulized budesonide (Pulmicort) 0.25 mg/2ml bid at home
g) follow-up in 24 hours by phone or return to office
B. Treatment for moderate and severe croup: transfer to ED via
ambulance; can start these treatments before transport if available
1. Work slowly and do not frighten the child, as this will make the
symptoms worse 2. Oxygen via cannula or mask (depends on what the
child will tolerate)
3. Nebulized epinephrine 1:1000 solution diluted in 3 ml normal saline or
premixed tubule of 0.5 ml 4. Oral dexamethasone 0.15 mg to 0.6 mg/kg
up to maximum dose of 10mg, as a single dose (made by mixing the
IM preparation [4mg/ml] in a cherry-flavored syrup) 5. Cool mist
humidifier if available

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Epiglotitis

I. Description: a viral infection with sudden-onset of acute inflammation and edema of glottic
structures.
II. Signs and symptoms: begins with fever (102.2°F up to 105°F), stridor, and labored breathing;
other signs include

A. Drooling, dysphagia, sore throat, and refusal to eat

B. Muffled voice (not hoarse) and minimal cough
C. The child appears quite ill with restlessness, irritability, and anxiety
D. Tripod sitting position with mouth open to facilitate breathing
III. Treatment is emergent transfer to ED via ambulance. DO NOT ATTEMPT VISUALIZATION
without intubation equipment readily available.

Respiratory syncytial virus (RSV) infection

I. Description: an acute viral lower respiratory tract infection primarily seen in children aged <4
years.
II. Signs and symptoms

A. Low-grade fever
B. Cough, tachypnea, intercostal retractions with wheezing and crackles
C. Cyanosis in very young infants with possible sepsis and apneic
episodes
D. May have associated OM
E. Dehydration with dry mucus membranes
III. Treatment is supportive

A. Increase humidity and fluid intake

B. Rest; analgesia for discomfort (see Tables 17-2 and 17-3) C.
Levalbuterol (Xopenex) nebulized solution 0.31 to 0.63 mg/3 ml tid or
albuterol nebulized solution 0.63 to 2.5 mg/3 ml tid D. Budesonide 0.25
to 0.5 mg/3 ml nebulized solution qd
E. Transfer emergently to ED via ambulance if the patient appears acutely
ill with difficulty breathing, lethargy, and is unable to keep fluids
down; O2 supplementation while awaiting ambulance F. Prophylaxis
for premature newborns or those with bronchopulmonary dysplasia:
consider Synagis

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Community-acquired pneumonia

I. Signs and symptoms

A. Child appears ill, with decreased activity and pulse oximetry <90% on
room air B. Dyspnea with intercostal retractions, productive cough
with rales, or decreased breath sounds over the pneumonia site; fever
usually ≥ 102.2°F and occasional N/V/D
C. Chest pain, abdominal pain, irritability
D. Fatigue and loss of appetite
E. Can have tachypnea, nasal flaring, intercostal retractions, grunting
II. Diagnostic testing

A. CBC may show elevated WBCs with a shift to left

B. CXR may show the area of pneumonia (or may not, if pneumonia has
not consolidated)
III. Treatment

A. Immediate transfer to ED for signs of respiratory distress: tachypnea

>60 with intercostal retraction, grunting respiration, cyanosis, flaccid
appearance, or child <5 years. If treated as an outpatient: supportive
care with increased humidity, increased fluids, rest, and antibiotic
therapy for 7 to 10 days
1. Amoxicillin/clavulanate <3 months of age: 30 mg/kg/day ÷ q12h; >3
months of age, <40 kg: 25 to 45 mg/kg/day ÷ q12h; >40 kg: use adult
dosing 2. Cefuroxime axetil 3 months to 12 years: 30 mg/kg/day ÷ q12h
3. Clarithromycin 2 months to 12 years: 15 mg/kg/day ÷ q12h
4. If allergic to penicillins and macrolides, doxycycline >8 years of age: 2 to
4 mg/kg/day divided q12h
B. Children aged < 12years may benefit from albuterol 0.63 to 2.5mg/3ml
or levalbuterol 0.31 to 0.63mg/3ml nebulizer solution tid until
respiratory symptoms improve (children aged > 12 years use adult
dose) C. Acetaminophen or ibuprofen for pain and fever (see Tables
17-2 and 17-3) D. Follow-up in office in about 24 to 72 hours; if not
improving, refer to ED

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Abdominal disorders
Pyloric stenosis

I. Description: hypertrophy of the pyloric sphincter, leading to obstruction

II. Signs and symptoms are not present at birth, but usually start at about 4 to 8 weeks of age

A. Nonbilious emesis with vomiting after feeding, which progressively

worsens and becomes projectile; even trial of small frequent feedings
worsens vomiting B. May have dehydration and weight loss
C. Poor feeding habits; the infant appears hungry after emesis and
during the day D. Will be lethargic and irritable with progression of
stenosis
E. Has a visible peristaltic wave traversing the epigastrium left to right
and a palpable “pyloric olive” sized mass to the right of the umbilicus
just below the liver edge (more prominent after vomiting)
III. Diagnostic testing if symptoms are not severe

A. Abdominal ultrasound (best test) or UGI

B. CMP may show metabolic alkalosis and electrolyte imbalance with
decreased K+ and Na+
IV. Treatment: transfer to a surgeon if stable and emergent referral to ED if dehydration is noted

Intussception

I. Description: telescoping of one bowel segment into another, most commonly at the ileocecal
valve II. Signs and symptoms

A. Sudden, acute abdominal pain; and vomiting (especially after viral

illness) B. Colicky, abdominal pain characterized by drawing up knees
and stiffening legs C. Bloody or “currant jelly” stools several hours
after the onset of pain
D. Sausage-shaped mass in the right upper quadrant
E. Fever, lethargy, and shocklike state
III. Treatment: emergent transfer to ED

Gastroenteritis

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I. Description: may be viral (usually norovirus; seen more often in winter), bacterial (seen more
often in summer), or parasitic; can be caused by antibiotics, drinking from streams or rivers, or
traveling to areas endemic for diarrheal diseases
II. Signs and symptoms

A. Acute onset N/V/D with abdominal pain/cramping and hyperactive

bowel sounds B. Dehydration signs (see Table 17-1) and weight loss;
increase in thirst C. Fever, chills, myalgias, rash, rhinorrhea, sore
throat, and cough (may indicate bacterial infection)
III. Diagnostic testing

A. CBC for anemia

B. CMP for electrolyte imbalance
C. Stool for O&P, culture, and C. diff
D. Urinalysis for infection
IV. Treatment for mild-to-moderate dehydration: oral rehydration solution (see Table 10-5) for
children <2 years old: ∼500 ml/day; for children 2 to 10 years old: ∼1000 ml/day; for children >10
years old: ∼2000 ml/day

A. Return to normal diet as soon as possible; if breast-feeding, try to

increase the number of feedings qd B. Probiotics qd for at least 1
month
C. No antimotility drugs
D. Decrease whole milk for 48 hours; may use diluted skim milk or
lactose-free formula E. Follow-up in office in 24 hours
V. Treatment for severe dehydration: emergent transfer to ED

Encopresis

I. Description: a syndrome with repeated stool incontinence, usually because of constipation

without an organic problem; more common in male than female patients II. Caused by a cycle of
constipation: pain with BM that leads to withholding stool, which causes the colon to enlarge,
allowing a larger holding capacity and eventually a decreased sensation to defecate; as the stool
backs up, liquid stool will leak out III. Signs and symptoms

A. Stool leakage with or without knowledge of the event

B. Anorexia; abdominal pain and distention; may palpate a soft,
nontender mass in the left lower quadrant C. Stools are hard, dry, and
large with increased straining when defecating, leading to anal fissures
D. Rectal examination may indicate decreased anal tone with large

614
 rectal vault or rectal stenosis; may have large amount of stool in rectal
vault
IV. Treatment is aimed at stopping the “hard stool-pain cycle” with a program developed to help
the child gain control of stooling

A. Phase one: disimpaction of the colon

1. Fleet enemas (based on age) for immediate results or
2. Milk of magnesia 2 to 6 years give 5-15ml/day; 6 to 12 years give 15-30
ml/day; >12 years give 30-60ml/day, or polyethylene glycol ≥6 months
give 0.5 to 1.5 mg/kg/day
B. Phase two: goal is BM 1 to 2 times qd
1. Use daily fiber (e.g., Benefiber or Metamucil) and daily laxatives (e.g.,
polyethylene glycol, sorbitol) 2. Allow time to stool after meals
3. Increase fluid intake and exercise
4. May need stool softening agents for years to prevent recurrence
C. Behavioral counseling may be needed to help with anxiety and pain
with stooling D. This process may take up to 6 months and relapse is
common

Gastroesophageal reflux disease

I. Description: commonly caused by delay in neurological maturation or diminished or reduced

sphincter pressure and esophageal clearance; crying, coughing, or defecating may also lead to
GERD in infants and children. This is common in premature infants up to age 6 months; it
usually resolves by 1 year of age but may persist into adulthood.
II. Signs and symptoms

A. Spitting-up or vomiting, usually after a meal

B. Chronic cough, wheezing, asthma, apnea
C. Sore throat, hoarseness, laryngitis
D. Bradycardia
E. Halitosis, dental erosions
F. Sinusitis, otitis media
G. Signs of concern
1. Recurrent vomiting, hematemesis, fever

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 2. Weight loss, failure to thrive, lethargy
3. Abdominal distention/pain, constipation, diarrhea
III. Diagnostic testing: CBC (e.g., anemia); CMP (e.g., electrolyte imbalances); urinalysis (e.g.,
infection) IV. Treatment

A. Nonpharmacologic treatment
1. If the baby is formula fed, switch to a hypoallergenic formula or add 1
T. rice cereal to 1 to 2 oz of formula 1 to 2 times qd 2. Increase number
of feedings and decrease the amount of each feeding
3. Infant: put in a portable carrier after meals (if using a carrier, put a
small pillow under the buttocks to keep hips extended, which prevents
increase in gastric pressure) 4. Older infant/child: elevate HOB and
sleep on the left side; position with pillows 5. Avoid exposure to
second-hand smoke
6. Limit foods that can worsen reflux (e.g., caffeine, chocolate, and fried,
fatty, or spicy foods) and encourage small, frequent meals 7.
Encourage weight loss and increase physical activity if the child is
obese
B. Pharmacological treatment
1. PPIs are considered first-line treatment after endoscopic evaluation;
approved for age >1 year; should be given 30 minutes prior to meals
a) omeprazole 1 mg/kg/day divided q12h
b) lansoprazole 15 to 30 mg qd
2. H2 blockers are considered second-line treatment
a) famotidine (Pepcid) 40 mg/5 ml
(1) <3 months of age: 0.5 mg/kg qd
(2) 3 to 12 months: 1 mg/kg/day ÷ bid
(3) 1 to 16 years: 1 to 2 mg/kg/day ÷ bid (not to exceed 40 mg bid)
b) ranitidine (Zantac) 15 mg/ml
(1) full-term infants: 1 to 4 mg/kg/day ÷ q8-12h
(2) 1 month to 16 years: 5 to 10 mg/kg ÷ bid
C. Follow-up should be approximately 2 to 4 weeks; consider referral to
pediatric gastroenterologist if symptoms persist

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Genitourinary tract disorders
Hypospadias

I. Description: a congenital deformity in which the urinary meatus is located on the ventral side
of the penis, most often on the glans; may be related to other congenital deformities II. Signs and
symptoms

A. Abnormal urinary stream with spraying of urine and difficulty with

stream; all depends on where the meatus is located on the penile shaft
B. Chordee causing a ventral curve in the penis with erection can be
seen in infants
III. Treatment: refer to a pediatric urologist

Cryptorchidism (undescended testicle)

I. Signs and symptoms: unable to palpate the testis in the scrotum after several attempts; have
the child sit in “tailor fashion” and observe testicles while the child is at rest; both testicles should
be seen and can be palpated; if not, note unilateral or bilateral absence of testicle II. Undescended
testicle must be distinguished from retractile testis and note should be made regarding unilateral
or bilateral undescended testicle III. Referral to a pediatric urologist for unilateral undescended
testis by age 6 months; refer to a pediatric endocrinologist or genetics specialist if bilateral
undescended testes are identified

Enuresis

I. Description

A. Intermittent involuntary urinary incontinence occurring a minimum

of twice weekly while sleeping in children aged >5 year
1. Primary enuresis: child was never dry
2. Secondary enuresis: child was dry and now is incontinent of urine
B. Daytime continence: usually achieved by 18 to 24 months; in 80% of
children by age 28 months C. Nighttime continence: usually achieved
by 6 years of age
II. History: FH of enuresis; question regarding potential for sexual abuse or illness related to
timing of onset of enuresis; when urination occurs and what are the school rules for bathroom
breaks; is there any concern for bullying when away from home
III. Physical examination is usually negative, but evaluation of genitalia is important for growth
and development of sexual characteristics; evaluate musculoskeletal growth, anal sphincter
control, and any abnormal masses in the genital area; swollen tonsils or snoring which might

617
indicate OSA IV. Diagnostic testing

A. Urinalysis (e.g., for infection)

B. Ultrasound of the bladder for emptying dysfunction
V. Treatment

A. Nonpharmacologic treatment
1. Supportive attitude for parents and child with the understanding that
usually the child will outgrow the condition 2. Educate the parents and
child how to strengthen the bladder muscle by urinating on schedule
during the day and gradually lengthening time between urination
times; encourage voiding at hs 3. Nighttime alarms may be helpful
(commercial products are available)
4. Decrease liquid intake after 6 PM and void before sleeping
B. Pharmacologic treatment
1. Imipramine (Tofranil) increases bladder capacity and sphincter tone; if
the child is >6 years, start with the lowest dose of 10 to 25 mg about 1
hour before hs; may increase if needed, not to exceed 50 mg; monitor
ECG annually for dysrhythmia 2. Desmopressin (DDAVP) acts as a
antidiuretic; >6 years of age: 0.2 to 0.6 mg/day orally about 1 hour
before bedtime; intranasal may increase the risk of water intoxication
and is not recommended 3. Oxybutynin and Oxybutynin XR for
children who may have small bladder capacity
a) >5 years of age: (immediate release) 5 mg bid to tid; (maximum dose
15mg/day) b) >6 years of age: (extended release) 5 mg qd (maximum
dose 20mg/day)
4. Try to wean off therapies q6-12mo and refer if no improvement; may
need further testing

Urinary tract infection

I. Causes: commonly caused by Escherichia coli secondary to fecal contamination and poor
hygiene

A. Consider UTI in
1. Any infant with unexplained fever
2. Toddlers with sudden-onset V/D and lower abdominal pain

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 3. Older children who were previously potty trained and are now
incontinent with or without urinary complaints (e.g., frequency,
abdominal or back pain, dysuria) 4. Adolescents usually exhibit same
signs as adults with frequency and dysuria
II. Signs and symptoms

A. Ill-appearing infant/child with fever >102.2°F for more than 48 hours

B. May have suprapubic pain; examine genitalia for any unusual redness
or ulcerations noted in the diaper area or vulvovaginal area (may be
due to poor hygiene) C. Observe for phimosis in boys and labial
adhesions in girls
III. Diagnostic testing

A. Urinalysis either by clean catch (with parent’s assistance) via a

pedibag or container or a catheter specimen; may be positive for
leukocyte esterase and nitrite; microscopic examination may show
WBCs >10/hpf and positive bacteria (any amount) B. Urine culture is
the standard test for UTI; positive result if:
1. Clean catch specimen: >100,000 CFU/ml of any bacteria
2. Catheterized specimen: >50,000 CFU/ml of any bacteria; if growth
between 10,000-50,000 CFU/ml present, repeat test and if >10,000
CFU/ml and presence of pyuria on dipstick, then treat for UTI 3.
Suprapubic specimen: any bacteriuria is considered positive for UTI
C. Consider renal/bladder U/S on all febrile infants/children aged 2-24
months
IV. Treatment

A. Pharmacologic treatment: for 3 to 5 days if the patient is afebrile and

immunocompetent; give for 10 days if febrile; treat empirically while
waiting for culture results
1. TMP-SMZ suspension >2 months of age: 8 mg/kg/day q12h (check for
resistance in your area) 2. Cephalexin >3 months of age: 25 to 40
mg/kg/day ÷ q6-8h
3. Cefixime (Suprax) 6 months to 12 years, ≤50 kg: 8 mg/kg once qd; >50kg ;
400mg qd 4. Nitrofurantoin 1 months to 12 years: 5 to 7 mg/kg/day ÷ q6h
(not for children with possible renal disease)
B. Nonpharmacologic treatment

619
1. Follow-up in 24 to 48 hours and repeat urinalysis in 1 to 2 weeks after
finishing antibiotics 2. Increase fluid intake; decrease
carbonated/caffeinated drink and juice intake 3. Drink cranberry juice
at hs; may be prophylactic
4. Discourage bubble baths
5. Encourage all-cotton underwear and removal of wet clothing and
swimsuits immediately after use 6. Good perineal hygiene
C. Urgent transfer to ED if the patient appears toxic, is not feeding or
taking fluids, is <3 months of age, has vomiting, or has fever >100°F
with evidence of recent UTI D. Refer to a urologist:
1. First UTI in boys and second UTI in girls; consider renal ultrasound: if
normal, a referral may not be necessary unless recurrent UTI 2. All
children with gross hematuria

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Musculoskeletal system disorders
Scoliosis

I. Description: a spinal deformity with a lateral curvature of the spine combined with vertebral
rotation that is initially painless and usually does not cause disability; if slight, the child may not
think anything is wrong and may only notice that clothing does not fit correctly
II. Screening: early screening physical examinations should start in the fifth to seventh grades (10
to 12 years of age in girls and 13 to 14 years of age in boys)

A. Maintain privacy, use good lighting, and for optimal results, use an
inclinometer/scoliometer to determine the amount of angle present B.
Have the child stand in front of you with minimal clothing and
observe the posture and physical proportions. The child’s head should
align over the sacrum; observe the shoulder height, scapula position
and prominence, waistline symmetry, and levelness of the pelvis.
1. Deviation represents curvature, especially with asymmetry of the
scapula, waistline, or rib humps 2. A tall, thin person may have
Marfan syndrome if scoliosis occurs with long sweeping right thoracic
curve and left lumbar curve, pectus excavatum, and arm span greater
than height
C. Adam forward-bending test with the child standing is a good test to
determine vertebral rotation:
1. Have the child bend forward at the waist while standing with feet
together and elbows straight with palms together; view the child’s
back from the side and back; a visible rib hump is caused by convexity
of ribs and suggests vertebral rotation 2. Inspect the chest for
deformity in the rib cage or sternum
D. Full spinal x-rays are needed to confirm scoliosis with Cobb angle test
for degree of angle and to denote where the curvature(s) is located
(most common is the right thoracic curve) E. Refer to a pediatric
orthopedist with any of the following:
1. The x-ray or school or office screening shows possible scoliosis with a
≥7° curve noted on the scoliometer during the forward-bending test 2.
New onset of curvature
3. Worsening curve noted in a child <12 years old

621
Limping child

I. Description: the patient is noted to have asymmetrical gait and increased clumsiness while
walking or running and may or may not have pain; may have questionable discrepancy in leg
length II. History

A. Obtain from the parent and child any history of recent illness, chronic
diseases or trauma B. Onset of pain, pattern of pain and gait changes,
fever or night sweats
C. Questions to ask
1. What provokes limp or pain and what makes it better; have any
medications been tried?
2. What does the pain feel like (e.g., sharp, dull, or burning) and does it
limit the child’s activity?
3. Does the pain stay in one place or radiate; where does the pain radiate?
4. Is the pain continuous or intermittent and how long does it last; has it
affected sleep?
III. Causes

A. Child of any age: injury, infection, inflammatory disease, tumor,

congenital deformity, Legg-Calve-Perthes disease, slipped capital
femoral epiphysis, and nervous system disease are possible B.
Children aged < 3 years: occult fractures, developmental dysplasia of
the hip, hip infection, and congenital leg length discrepancy C.
Children aged 5 to 10 years: juvenile RA, synovitis, and Legg-Calve-
Perthes disease are common D. Children/adolescent aged 11 to 18
years: slipped capital femoral epiphysis, avascular necrosis of the
femoral head due to trauma, overuse injury, Osgood-Schlatter disease,
or possible gonococcal septic arthritis are common
IV. Physical examination

A. Observe the patient while walking and running and note coordination
and how the feet move; observe for foot flapping and toe walking;
examination is easier if the child is clothed only in shorts and t-shirt B.
Inspect and palpate all joints, especially the hips and lower extremities
for any pain, limited ROM, bruising, redness, or swelling C. Inspect
the patient posteriorly for discrepancy in gluteal and thigh skin folds
and assess toddlers/children for positive Trendelenburg gait D. Test
for Trendelenburg gait: have the child stand on the affected limb and

622
 lift the unaffected limb from the floor; positive test shows that the
pelvis does not stay level but drops down toward the unaffected side
(consider hip dysplasia) E. Test for loss of hip abduction: place the
infant/child on the back with hips/knees flexed and toes placed
together and allow both knees to fall outward; if the affected leg will
not abduct as far, consider hip dysplasia F. Assess for leg length
discrepancy: the child is supine with the knees bent and feet flat on the
bed; assess the height of the knees; if asymmetrical, there is leg length
discrepancy G. Assess the neurological system (see Chapter 2) for
neurological diseases
V. Diagnostic testing

A. X-ray of the affected extremity with bilateral comparison views

B. Consider bone scan or MRI
C. CBC and inflammatory markers (e.g., ESR, CRP) including lyme titer;
alkaline phosphatase and calcium
VI. Treatment: refer to a pediatric orthopedist

Developmental dysplasia of the hip (DDH)

I. Description: imperfect hip joint development affecting the femoral head and/or acetabulum; if
untreated, will lead to immobility of the affected joint. May be hereditary, related to breech birth
(14 times greater incidence), or due to capsular laxity; most often seen in females and the left hip
is the most commonly affected hip II. Signs and symptoms

A. If not treated early, can be the cause of OA and hip joint replacement
in an adult B. Birth to 3 months of age
1. Can range from instability in newborn examination to subtle limited
abduction in an infant
2. Assess using Barlow maneuver, which causes the hip to dislocate
3. Assess using Ortolani maneuver, which reduces the joint and a
“clunk” or “click” is felt 4. Assess for shortening of femur with
unequal knee heights
C. Older infant
1. The leg on the affected side may turn outward
2. Limitation of hip abduction in 90 degrees of flexion
3. Asymmetry of skin folds (e.g., thigh, gluteal or popliteal)

623
 4. Leg length asymmetry with unequal knee heights when supine and
knees flexed with shortening of the femur on the affected side 5. Lax
hamstrings
D. Walking child
1. Nonpainful asymmetric gait in a toddler
2. Scoliosis
3. Leg length discrepancy with out-toeing and genu valgum
4. Prominent greater trochanter on the affected side
5. Trendelenburg gait
6. Excessive lordosis
E. Adolescent
1. Slow, insidious onset of pain, which is worse with activity or sports
2. Increased difficulty with gait, subtle Trendelenburg sign, limping
3. Occasional “locking” or “catching” of the affected hip
4. Pain is located in the groin or anterolateral aspect of the hip but can be
felt in the anterior aspect of the thigh
III. Diagnostic testing

A. X-rays of the hip should include frog leg and lateral views; entire
lower legs if the child is unable to localize pain B. U/S of the joint to
assess for effusion
IV. Treatment: refer to a pediatric orthopedist

Congenital talipes equinovarus (club foot)

I. Description: a congenital condition that should be corrected/treated early to prevent

complications later in life II. Signs and symptoms: forefoot abduction and inversion with the
ankle in plantar flexion that cannot be easily straightened out III. Treatment: refer to a pediatric
orthopedist

Patellofemoral pain syndrome (chondromalacia patellae)

I. Description: a common cause of knee pain related to abnormal biomechanics, soft tissue
tightness and muscle dysfunction; seen most often in teens, athletes II. Signs and symptoms

A. Pain under or around the patella where it attaches to the femur, which
worsens with flexion against resistance or flexion with prolonged

624
 sitting and may have sensation of “giving way” or buckling with
activity B. Dull ache in anterior knee with flexion/extension activity
(e.g., going up/down stairs), crepitus that causes pain with knee
motion
III. Diagnostic testing: x-ray of the knee if trauma was involved
IV. Treatment

A. Stop activity that causes pain and rest the extremity and then restart
activity slowly B. P.T. to evaluate and treat and for muscle
strengthening and reconditioning C. NSAIDs and ice may be of use in
acute inflammatory situations
D. Refer to an orthopedist or sports medicine clinic if the pain does not
resolve with conservative treatment

Osgood-schlatter disease
I. Description: painful, self-limiting tibial tubercle swelling involving the patellar tendon where it
attaches to the tibia; usually starts in adolescence and is associated with overuse activity (e.g.,
heavy sports involvement) II. Signs and symptoms

A. Knee pain with swelling and tenderness below the patella

B. Usually develops over time (i.e., not acute) and does not cause
permanent disability C. Most symptoms will completely resolve after
the bone stops growing in 2 to 3 years; some may have swelling over
the patellar tendon indefinitely but no pain
III. Treatment

A. Conservative treatment with ice for 20 minutes 5 to 6 times qd

B. NSAIDs for pain relief (may not shorten the course)
C. Avoidance of pain-producing activity; use knee immobilizer for
support (both decrease activity, help healing) D. Quadriceps and
hamstring stretching exercises may reduce tension on the tibial
tubercle
IV. Refer if the symptoms are not improving or if antalgic gait, swelling with redness/heat, or
fever develops

625
Hematopoietic system disorders
Iron-deficiency anemia (IDA) (see chapter 9)

I. Description: the most common nutritional deficiency found in infants and children II. Causes:
inability to meet iron needs secondary to rapid growth, poor intake of iron-fortified
foods/formulas, predominant whole milk diet (i.e., microscopic blood loss from the GI tract) III.
Signs and symptoms

A. Pica; irritability
B. Pallor, fatigue, blue sclera
C. Refusing solid foods, poor feeding habits, and anorexia
D. Delayed development if anemia persists
E. Increased number of infections
IV. Diagnostic testing

A. Screening Hgb/Hct can be considered at 9 months of age, between 12

to 24 months of age, and between 11 to 15 years of age
B. If anemia suspected, consider additional testing (see Chapter 9, Iron
Deficiency Anemia) C. Lead level testing at 12 and 24 months of age or
if lead exposure is suspected
V. Treatment

A. Breast-fed infant: start supplementation at 4 months of age with

1mg/kg/day of oral iron until intake of iron foods is adequate to
maintain iron levels (see Appendix for list of iron fortified foods) B.
Formula-fed babies should receive iron-fortified formulas and then
start iron-fortified foods at 4 months of age (see Appendix for list of
iron fortified foods) C. Toddler: if not receiving iron-fortified foods
(see Appendix), should be given supplementation with vitamins or
oral iron supplements (e.g., OTC ferrous sulfate) to maintain intake at
around 11 mg/day of elemental iron
1. Toddlers between 1 to 3 years of age need ∼7 mg/day from oral
intake; if not provided, oral supplementation is available 2. Children
aged >3 years need ∼ 10mg/day with high iron foods or chewable
vitamins with extra iron 3. Limit whole milk intake in toddlers <2
years of age to ∼24 oz qd; whole milk is irritating to the colon and

626
 causes chronic iron loss
D. Adolescents: monitor closely due to dietary restrictions (e.g., self-
induced), history of anemia, or heavy, irregular menstrual cycles;
rapid growth at this age will deplete iron stores faster than
replacement can occur
1. Supplementation with multivitamins with iron (e.g., Flintstones with
iron 2 qd) or ferrous sulfate OTC 1 to 2 tabs qd with orange juice
(vitamin C enhances the absorption of iron) and increased iron-rich
foods (see Appendix) should correct anemia in healthy adolescents 2.
Iron is best absorbed on an empty stomach; antacids, milk products, or
caffeinated beverages decrease uptake
E. Follow-up CBC should be done at 1 to 2 months after starting
treatment
F. Refer to hematologist if anemia does not improve with adequate iron
replacement

627
Gynecological disorders
Labial adhesions

I. Description:

A. Most common in female children between 13 to 23 months of age after

circulating estrogen hormones from birth have started to decline B.
Not seen in newborns because of increased circulating maternal
estrogen
C. May be caused by chronic bubble baths, harsh soaps, overcleaning
after diaper changes
II. Signs and symptoms

A. Local inflammation, recurrent vulvovaginitis, or recurrent UTIs

B. Adhesion of the labia minora starts posteriorly into the fourchette and
progresses toward the clitoris; the vaginal opening may not be
visualized C. The skin is pale and dry
D. The urethral opening should be present
III. Diagnostic testing with ultrasound should be considered if genital anomalies, masses, or
fusion of the labia majora are present; these may be indicative of absence of the uterus or of
ambiguous sexual organs IV. Treatment

A. DO NOT forcefully try to separate the labia

B. Watchful waiting is recommended; this may resolve spontaneously by
1 year of age C. If treatment is indicated, apply a topical estrogen
cream to the labial adhesions 1 to 3 times qd for several weeks until the
adhesions start to resolve; the frequency of application can be
decreased as the adhesions improve D. Once the labia separate, use
emollient cream (e.g., A&D ointment or Aquaphor) 3 to 5 times qd for
several months to allow healing and prevent recurrence E. Refer to a
pediatrician or pediatric gynecologist if the adhesions do not resolve

Vulvovaginitis

I. Description: inflammation to the vulva/vagina secondary to infection involving the lower third
of the vulva; common in prepubertal children II. Common causes

A. Poor perineal hygiene, improper wiping after BM, and tight clothing

628
 B. Irritation from bubble baths; dirt or sand from sandbox imbedding in
the folds of the labia or groin C. Insertion of foreign objects into the
vagina
D. Hypoestrogenic state
E. Bacterial infections caused by Streptococcus, H. influenzae, E. coli,
Staphylococcus, C. trachomatis, N. gonorrhea or Trichomoniasis F. Sexual
abuse
G. Pin worms, scabies or lice
III. Signs and symptoms

A. Burning, itching, discharge, bleeding, dysuria

B. Labia may be excoriated and red with rash or bruising
C. Vaginal discharge
1. If foul odor, suspect a foreign object
2. Yellow color, suspect skin infection from scratching
3. White discharge without odor, suspect Candida
4. With associated labial thickening, suspect a foreign object
IV. Diagnostic testing should include the following

A. STI testing with a wet prep

B. Anaerobic and aerobic culture for specific bacteria or Candida (Candida
is rare in children unless they are immunocompromised) C. Urinalysis
for occult infection (obtain a catheter specimen to avoid vaginal
discharge contamination of the urine specimen)
V. Treatment

A. Proper hygiene and avoidance of irritants (e.g., bubble baths, scented

peripads) B. Sitz baths with cool water to ease itching and pain
C. All-cotton clothing; do not leave wet clothing or bathing suits on for
any length of time D. Nonmedicated ointment to protect the vulvar
skin (e.g., Vaseline)
E. May need OTC hydrocortisone cream to relieve itching and decrease
irritation F. Consider antibiotic treatment for 7 to 10 days, especially if
there is purulent vaginal discharge
1. Cephalexin 25 to 50 mg/kg ÷ tid

629
2. Amoxicillin 25 to 50 mg/kg bid
G. Referral to a pediatric gynecologist for further evaluation, possibly
under anesthesia, to identify the cause

630
Neurological disorders
Attention-deficit hyperactivity disorder (ADHD) and attention
deficit disorder (ADD)

I. Description: defined by developmentally inappropriate degrees of inattention, impulsiveness,

and hyperactivity

A. Parental reports of child’s behavior and symptom duration of at least

6 months with onset before age 12 years; inattentive, hyperactive, or
impulsive symptoms must occur in at least two settings B. If the child
exhibits at least two of the following, recommend standardized testing
with a psychologist trained in this type of testing
1. Often fails to finish projects and homework; does not pay attention to
detail and makes simple mistakes on school work 2. Often does not
seem to listen when spoken to directly
3. Easily distracted by extraneous stimuli and forgetful of scheduled
daily activities 4. Has difficulty concentrating on tasks; difficulty
organizing tasks; loses things necessary for completion of tasks 5. Is
always on the “go” and often acts before thinking and goes from one
activity to another rapidly 6. Unable to take part in leisure activities
7. Oftentimes interrupts or intrudes into others’ personal space
8. Needs a lot of supervision for completion of projects, cannot stay
seated, and talks excessively
II. Diagnostic testing includes CBC, TSH, and lead screening
III. Treatment

A. Pharmacologic treatment:
1. Amphetamine stimulant: dextroamphetamine/amphetamine
(Adderall)
2. Methylphenidate stimulant: Ritalin, Concerta
3. Nonstimulants
a) atomoxetine (Strattera) >6 years, <70 kg: 0.5 mg/kg/day; >6 years, >70 kg
: 40 to 80 mg qd b) guanfacine (Intuniv) 6 to 17 years: 1 to 4 mg/day;
adjust the dose depending on age and size

631
4. Antidepressants
a) bupropion (Wellbutrin) > 6 years: 1.4 to 6 mg/kg/day
b) paroxetine (unlabeled use) 7 to 17 years: 10 to 20 mg/day
5. Miscellaneous: clonidine is dose dependent on age and weight
B. Education
1. Review monitoring routines for medications and appointments
2. Citric acid and vitamin C significantly impair the absorption of
stimulants; do not ingest products containing these agents 1 hour
before or after medication (e.g., citrus fruit and juice, toaster pastries,
most carbonated beverages, granola/breakfast bars, high-vitamin
cereals, oral suspension medicines) 3. Teach parents behavioral
modification techniques and encourage firm, realistic, and
environmental limits 4. Refer for special education, if needed
C. Refer to a psychologist or psychiatrist for further evaluation or
treatment.

632
Cardiac disorders
Hypertension

I. Description: BP guidelines are based on the National Heart, Lung, and Blood Institute (NHLBI)
(www.nhlbi.nih.gov) guidelines

A. Normal BP: systolic and diastolic pressure readings are <90th

percentile B. Pre-HTN: BP >90th percentile but <95th percentile or
adolescents BP >120/80 mmHg even if <90th percentile C. HTN: either
systolic or diastolic pressures are >95th percentile on three or more
readings; in patients aged <18 years, both readings are significant D.
Must take minimum of three readings to determine if HTN is present
when the child is not ill
II. Signs and symptoms: usually asymptomatic, but could have H/A, blurred vision, irritability,
nosebleeds, and poor school performance III. Diagnostic testing

A. CBC, CMP, lipid profile, TSH, U/A, and urine protein/creatinine ratio
B. Consider CXR, renal U/S
C. Echocardiogram
D. Consider sleep study for OSA
IV. Treatment for essential HTN

A. Emergent transfer with hypertensive crisis with any symptoms such

as headache, dizziness, or chest pain B. Referral to a pediatric
cardiologist for evaluation initially if there is no identifiable cause for
HTN and then co-manage; referral within 1 week if BP >99th percentile
plus 5 mmHg C. Lifestyle changes for stage 1 HTN without target
organ damage (see Chapter 8, Hypertension, IV) D. Ambulatory
monitoring
1. Pre-HTN: BP readings every 6 months
2. Stage 1 HTN with lifestyle changes: monitor BP every month (or more
often if needed)
E. Preparticipation sports requirements: may play sports if controlled BP
is documented on three different occasions

633
CHAPTER 18

634
Psychiatric conditions
Initial office visit

I. Nurse practitioners must be constantly aware that as many as 50% of patients who are seen in a
primary care setting may have psychiatric symptoms and that depression is common with many
comorbid conditions (e.g., DM, CV disease, CVA, chronic pain, COPD, cancer). Many patients
may be unable to accurately describe physical symptoms or attribute them to psychological
issues/stressors that occur over a period of time; family interviews may be necessary to
determine the symptoms and behavioral changes.
II. History: in addition to the typical questions asked during a routine history, questions that at
times seem too personal but provide essential information may need to be asked. Patients and
families are often guarded in their answers because of embarrassment or fear of judgment.
Reassure the patient of confidentiality and of the importance of the questions, and then note the
following regarding the CNS to rule out an organic disease:

A. H/A: recent onset or change

B. Vision: recent deterioration, blurring, or spots in vision; hallucinations
C. Hearing: recent deterioration, other sensations, or changes (e.g.,
tinnitus, hearing voices)
D. Speech: any recent difficulty or change (e.g., muffled, garbled,
uncontrollable speech; does the patient ramble on or focus on the
topic? Does the patient swear, joke, or mimic another’s words or
actions?)
E. Writing: any recent difficulty or change from previous functioning
F. Memory: recent changes in both long-term and short-term memory
G. Gait: recent change or deterioration (e.g., shuffling, ataxia, waddling,
dragging a limb)
H. Dexterity: inability to grab objects, clumsiness
I. Sensation: any unusual sensations (e.g., things crawling on the skin,
fleeting burning pain, pins and needles)
J. Strength: recent weakness in any limb, asymmetric grip strength
K. Consciousness: history of blackouts or periods of time that cannot be
accounted for

635
 L. Body movements: uncontrollable body movements (e.g., tongue
biting, seizures)
M. Substance use: use of drugs or alcohol for anxiety, nervousness, relief
of symptoms, or other reasons; use of OTC or herbal products
III. Mental status interview: be alert for cues that something is not quite right (e.g., inappropriate
clothes, facial expression, verbal utterances, body language). Is the patient’s affect inappropriate
(e.g., laughing at sad events, weeping when others are happy)? During or after the history and
physical examination, a mental status interview should be conducted to determine if the patient
has delusions or a psychotic process; suggested questions include the following:

A. What brought you to the office today?

B. How are you feeling right now? How have you been feeling lately?
C. Have you noticed anything unusual in your thinking or behavior?
D. Have you experienced rapid mood swings (e.g., highs, lows)?
E. Are you troubled by any thoughts or feelings that pop up in your
mind and hang around?
F. Do you feel others are talking about you or judging you? Do you think
anyone is out to harm you?
G. Do you feel guilty for anything in your past or are you excessively
bothered by past events?
H. Do you feel the desire or need to harm yourself or others?
I. Have you considered suicide or do you hear voices telling you to harm
others or that you deserve to die? Have you thought of a plan for your
suicide?
J. Are there others you would like to harm or get revenge on? Do you
have a plan?
IV. Diagnostic tests: relevant tests for a psychiatric disorder should include the following:

A. CBC with differential and ESR

B. Complete chemistry panel, vitamin B12 levels
C. Thyroid function (with depressive disorders)
D. EEG (with seizures or sleep apnea)
E. ECG (for patients taking heart medications and elderly patients)
F. Urine HCG (when appropriate)

636
Mood disorders
Depression

I. Dysthymic disorder

A. Description: depressed mood on most days for at least 2 years; during

the depression period, also has at least 2 of the following:
1. Poor appetite or overeating
2. Insomnia or hypersomnia
3. Low energy or fatigue
4. Low self-esteem
5. Poor concentration/difficulty making decisions
6. Feelings of hopelessness
B. May have symptom-free periods, but not >2 months at a time
C. Treatment
1. Often has an early and insidious onset and is a chronic disorder; may
have concomitant medical disorders
2. Antidepressants have been effective in a majority of patients (see Table
18-1)
3. Counseling has been found to be beneficial for some patients
II. Major depression (adults)

A. Description: persistent depression that lasts at least 2 weeks and

includes ≥5 of the following symptoms, with one symptom being
either the first or second one:
1. Depressed mood most of the day nearly qd
2. Loss of interest or pleasure in usual activities (anhedonia)
3. Change in appetite or weight
4. Insomnia or increased need for sleep
5. Psychomotor agitation or retardation (not merely restless and unable to sit
still or feeling slowed down)

637
6. Fatigue or loss of energy
7. Feelings of worthlessness or excessive guilt
8. Poor concentration
9. Recurrent thoughts of death or suicide
B. Common physical symptoms
1. Exhaustion
2. Vague pain not related to any disease process and not reproducible;
H/A
3. Lump in the throat, nausea
4. Sexual complaints
C. Treatment
1. Cognitive therapy (counseling) can work as well as medications, even
for severe depression, and is more effective in preventing relapse
2. Standardized depression instruments (e.g., PHQ-9, which can be found
at www.phqscreeners.com/pdfs/02_PHQ-9/English.pdf) can help with
treatment decisions and monitoring progress. For medications, see
Table 18-1.
3. Treatment may also be needed for anxiety
4. Medications should be started slowly, and the dose should be titrated
up to the therapeutic level that resolves the symptoms. Titrate the dose
until the patient answers “yes” to the following questions: Are you
100% better? Are you again doing activities and hobbies that you enjoy
(i.e., enjoying life again)?
5. There is considerable variation in the amount of time required for
antidepressants to reach a therapeutic level: there may be improved
energy after ∼2 weeks, but mood effects may take 6 to 8 weeks
(although venlafaxine often eases symptoms faster)
6. The dose should be maintained at the therapeutic level for at least 1
year; patients with recurrent depression may need medication for life
7. A primary consideration with elderly patients is to distinguish
depression from other physical and mental diseases, especially
dementia and delirium (see Table 18-4)

638
8. Medication points
a) SSRIs are usually first-line treatment
(1) may cause hyponatremia, especially in elderly patients; check serum
sodium before starting and recheck in 1 month
(2) paroxetine can decrease cognition in elderly patients and cause
sedation; it is better for anxious, younger people; it may also cause
weight gain
(3) fluoxetine is not recommended for elderly patients because of its long
half-life but is safe in children
(4) SSRIs may cause sexual dysfunction in up to 50% of patients; treat
with a lower dose or change to a non-SSRI agent
(5) citalopram: do not use at a dose >20 mg qd in adults aged >60 years
(potential risk for QT prolongation)
b) with comorbid cardiac conditions, use sertraline (safe and effective
with CV disease); mirtazapine or bupropion may also be used alone or
in combination with sertraline
c) SNRIs
(1) venlafaxine has a rapid onset of action and is helpful for patients who
need an immediate boost (e.g., no energy or interest in activities)
(2) duloxetine is used for pain management (including DM neuropathy)
with/without depression
(3) venlafaxine and desvenlafaxine (Pristiq) are helpful for depression
with fatigue and/or exhaustion
d) use bupropion (Wellbutrin) for patients who are depressed and also
want to stop smoking
e) tricyclic antidepressants (TCAs)
(1) use cautiously in elderly patients because of anticholinergic side
effects (e.g., dry mouth, constipation, pupil dilation [worsens
glaucoma], increased heart rate, urinary retention); nortriptyline
(Pamelor) works for depression without anticholinergic effects
(2) tend to cause weight gain
(3) amitriptyline has potent α-blocking properties, which can result in

639
 orthostatic hypotension; it may be beneficial in hypertensive,
depressed patients
f) amitriptyline and trazodone are the most sedating antidepressants; use
in patients with insomnia; administer at hs; usual starting dose is
amitriptyline 10 to 25 mg or trazodone 50 mg
g) with resistant depression, try an SSRI plus bupropion or mirtazapine
h) never give fluoxetine and amitriptyline to the same patient;
amitriptyline is not metabolized and can become toxic
i) when changing meds: do a “next day” switch within the same class or
SSRI to SNRI (the exception is fluoxetine because of its long half-life—
wait 4 to 7 days after stopping it); do “cross-tapering” when switching
to a different class (titrate down the current med over a 1-to 2-week
period or longer and titrate up the new med at the same time)
j) St. John’s Wort: there is no consistent evidence of effectiveness and it
has many side effects and interactions with commonly used
medications; for these reasons, its use should be discouraged
k) mirtazapine can cause weight gain; this may be an advantage in
elderly patients with weight loss or poor appetite. Doses >15 mg qd
cause more sedation.
l) SSRIs, bupropion, and venlafaxine may worsen sleep, at least at the
start of therapy; have the patient take them in the morning
m) be aware of the many other medications that can cause depression
(e.g., propranolol, cimetidine, methyldopa, OCs, corticosteroids). Also,
long-term ETOH or marijuana use and cocaine or methamphetamine
withdrawal can cause depression.
9. Follow-up in 2 to 4 weeks, then again in 2 to 4 weeks, then in 1 to 2
months, then as indicated
10. Recurrent depression may result from inappropriate prescription of
medications at a dose too low for an inadequate trial period coupled
with poor follow-up. Consider referral for counseling or possible
hospitalization.
D. Referral
1. To a psychologist for counseling or cognitive behavioral therapy

640
2. To a psychiatrist or psychiatric NP with
a) no improvement or remission not achieved after adequate trial with 1
to 3 agents
b) comorbidities (e.g., psychosis, bipolar disorder, severe depression, or
dysthymia plus acute depressive episode)
3. To inpatient treatment or ED with suicidal/homicidal ideations
E. Patient and family education
1. Duration of depression (6 months to 2 years)
2. Chronicity and recurrences
3. Disability and intensity associated with depression
4. The patient does not choose to be depressed; at times, depression is
associated with a chemical imbalance
5. Expected side effects of the prescribed medications (particular side
effects for each patient cannot be predicted but will be treated)
F. Antidepressant withdrawal
1. TCAs: occurs from 24 to 48 hours up to 2 weeks after discontinuation
a) GI complaints with or without anxiety
b) sleep disturbances, paradoxical mania
c) movement disorders
2. SSRIs: timing depends on which is used (half-life varies)
a) dizziness, anxiety, paresthesias
b) nausea
c) insomnia, nightmares
3. MAOIs: comparable to opiate and amphetamine withdrawal
a) anxiety, paresthesias
b) H/A
c) muscle weakness, shivering
d) psychosis, delirium, hallucinations
4. Treatment

641
 a) withhold medicine in case of mild symptoms as they are temporary or
b) restart medicine and taper off over at least 2 to 4 weeks; may take up
to 2 months. If symptoms recur, consider a low dose of medicine for
several months and then re-try tapering off.
III. Seasonal affective depressive disorder (SADD)

A. Description: symptoms occur late fall through late spring and include
increased sleep, increased appetite with carb cravings, increased
weight, irritability
B. Treatment
1. Light therapy: there are commercially available devices; NOT tanning
beds
2. Medications (see Table 18-1)
IV. Major depression (pediatrics)

A. Signs & symptoms

1. Children overall exhibit more separation anxiety, somatic disorders,
auditory hallucinations, temper tantrums, and changes in behavior at
home and school
2. Children in middle-to-late childhood have more dysphoria, low self-
esteem, guilt, and hopelessness
3. Teens are more likely to have sleep and appetite problems (e.g.,
bulimia, anorexia), delusions, or OCD; they are at increased risk for
high-risk behaviors (e.g., promiscuity, smoking, alcohol and drug
abuse, suicide attempts)
4. A high percentage of patients have comorbid psych disorder (e.g.,
anxiety, substance abuse, ADHD, eating or learning disorder)
B. Diagnostics
1. Complete chemistry panel, TSH, CBC
2. Urine HCG (females)
3. Physical examination focus: identification of self-harming behaviors
(e.g., cutting, suicide attempts), drug abuse (IV tracts), signs of injury
(e.g., bruising from falls or physical abuse)
C. Treatment

642
 1. Refer to ED with suicide thoughts or intent
2. Refer to a pediatric psychiatrist or psychiatric NP for medication
management
3. Refer to/encourage counseling with a psychologist trained in pediatrics
Table 18-1
Antidepressant Therapy

Starting Maintenance Sexual Anticholinergic Approved

Drug Sedation
Dose Dose Dysfunction* Effect Uses
Selective Serotonin Reuptake Inhibitors (SSRIs)
Citalopram 20 mg 20-40 0 0/+ 0 Depression
(Celexa) qd
Escitalopram 10 mg 10-20 0 0/+ 0 GAD
(Lexapro) qd Depression
Fluoxetine 20 mg 10-80 0/+ 0/+ 0 Depression
(Prozac) AM Panic
disorder
OCD
Fluvoxamine 100 mg 100-300 ++ +/++ ++ OCD
(Luvox) hs
Paroxetine 20 mg 10-60 ++ ++++ 0/+ Depression
(Paxil) qd 12.5-62.5 OCD
(Paxil CR) 10 mg PTSD
qd GAD
(panic)
25 mg
qd
12.5 mg
qd
(panic)
Sertraline 50 mg 50-200 0 ++++ 0 Depression
(Zoloft) qd OCD
25 mg Panic
qd disorder
(panic PTSD
and
PTSD)
Serotonin Norepinephrine Reuptake Inhibitors (SNRIs)
Duloxetine 30-60 120 0 GAD
(Cymbalta) mg qd Depression
Desvenlafaxine 50 mg 100 + + 0 Depression
(Pristiq) qd
Levomilnacipran 20 mg 120 Depression
(Fetzima) qd
Venlafaxine 37.5 mg 75-225 0 +++ 0 Depression

643
 (Effexor, Effexor bid GAD (XR
XR) 37.5 mg only)
qd Panic
disorder

Tricyclic Antidepressants (TCAs)

Amitriptyline 25 mg 40-150 ++++ ++ ++++ Depression
(Elavil) hs to 25
mg tid
Desipramine 25 mg 50-300 + + + Depression
(Norpramin) hs to 25
mg tid
Doxepin 75 mg 75-300 +++ ++ ++ Depression
(Adapin, hs or 25 Anxiety
Sinequan) mg tid
Imipramine 75 mg 50-200 ++ ++ ++ Depression
(Tofranil) hs
Nortriptyline 25 mg 50-150 ++ ++ ++ Depression
(Aventyl, hs to 25
Pamelor) mg tid
Miscellaneous
Bupropion 100 mg 400-450 ++ ++ Depression
(Wellbutrin, bid SADD (XL
Wellbutrin SR 150 mg only)
and XL) qd (XL ADHD
only) (adult)
Mirtazapine 15 mg 15-45 +++ 0 ++ Depression
(Remeron, hs
Remeron Soltab)
Trazodone 50 mg 50-400 ++++ + Depression
(Desyrel) tid
*
Consider these options to help with sexual dysfunction, especially when it is a side effect of antidepressants: Ginkgo biloba 60-240 mg
qd; bupropion SR 150 mg qd, Viagra 50-100 mg taken 1 hour before intercourse.
0, none; +, slight; ++, moderate; +++, high; ++++, very high.

Serotonin syndrome

I. Description

A. A potentially life-threatening condition associated with alterations in

cognition and behavior, autonomic nervous system function, and
neuromuscular activity
B. Thought to be caused by increased or excessive serotonin activity and
may be related to taking >1 of the following:
1. SSRIs
2. SNRIs (e.g., venlafaxine, duloxetine, milnacipran)

644
 3. TCAs (e.g., amitriptyline, imipramine, doxepin)
4. Atypicals (e.g., trazodone, mirtazapine, vilazodone, bupropion)
5. MAOIs (more often associated with adverse outcomes, including
death)
6. Opiates (e.g., tramadol, meperidine, fentanyl, methadone)
7. “Triptans”
8. Some GI meds (e.g., metoclopramide, ondansetron [Zofran],
granisetron [Kytril])
9. Valproate, carbamazepine
10. Buspirone
11. Lithium
12. Antihistamines, first generation (e.g., chlorpheniramine,
diphenhydramine)
13. “Street drugs” (e.g., amphetamine, cocaine, LSD, MDMA [Ecstasy],
bath salts)
14. Herbs/supplements (e.g., St. John’s Wort, L-tryptophan,
dextromethorphan)
II. Signs and symptoms: suggested diagnosis based on taking a serotonergic med plus having
ONE of the following:

A. Spontaneous clonus (with rigidity usually greater in lower

extremities)
B. Inducible clonus plus agitation or diaphoresis
C. Ocular clonus plus agitation or diaphoresis
D. Tremor plus hyperreflexia
E. Hypertonia plus temp >100.5°F plus ocular or inducible clonus
III. Treatment

A. Mild cases: stop potential offending medications; usually self-limited

with complete recovery within a few days
B. More severe cases: emergency transfer to ED; treatment focuses on
supporting respiratory and cardiovascular systems

Bipolar disorder

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I. Description: characterized by episodes of mania, hypomania, and depression

A. Manic episodes involve clinically significant changes in mood,

behavior, energy, sleep and cognition; examples include the following:
1. Inability to sit still and intense overactivity in both body and mind
2. Speech pressure (often loud, inappropriate; often jumps from one
subject to another)
3. Mood lability (e.g., irritability, euphoria, suspiciousness)
4. Cognitive abnormalities (e.g., poor concentration, racing thoughts,
grandiosity, manipulativeness); psychosis with delusions and
hallucinations; sleeplessness
5. Hypersexuality
6. May be too hyperactive to eat or drink, causing fluid depletion and
weight loss
B. Episodes of major depression, hypersomnia, and weight gain follow
manic episodes
C. If considering bipolar disorder, may screen the patient using a Mood
Disorder Questionnaire (a good example can be found at
www.integration.samhsa.gov/images/res/MDQ.pdf)
II. Treatment

A. Refer to a psychiatrist or psychiatric NP; the patient may need

inpatient treatment, especially initially
B. Consider Seroquel XR until seen by a psychiatric provider; obtain
baseline CMP and lipids
C. When interviewing the patient, talk in a calm, nonjudgmental manner

Anxiety

I. Description: anxiety is a normal reaction if it is aroused by realistic danger, if the reaction is

appropriate to the threat, and if the anxiety disappears when the threat ceases. Anxiety that
exceeds this definition is outside the patient’s voluntary control and often renders the patient
unable to function. Anxiety is among the most disabling diseases and frequently is a comorbid
illness with depression, substance abuse, psychiatric disorders, and medical conditions.
II. Classification of anxiety disorders: the most common are generalized anxiety disorder (GAD),
panic disorder, and posttraumatic stress disorder (PTSD)
III. Signs/symptoms and treatment (according to the DSM-5 criteria)

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A. GAD
1. Diagnosis/signs and symptoms
a) GAD is ruled out if the patient answers “no” to “Do you worry
excessively about minor matters?”
b) excessive and persistent worrying about a number of things occurring
most days for ≥6 months. The patient has difficulty controlling the
worry.
c) associated with ≥3 of the following (only 1 is required in pediatrics):
(1) restlessness or feeling keyed up or on edge
(2) fatigued easily
(3) difficulty concentrating or remembering (e.g., “mind going blank”)
(4) irritability
(5) muscle tension
(6) sleep disturbance
d) the symptoms cause significant distress or impairment in patient’s life
e) the disturbance is not the result of a substance (e.g., drug abuse) or
other medical condition (e.g., hyperthyroidism)
2. Treatment
a) an individualized plan combining the following: cognitive behavioral
therapy, medications, long-term follow-up
b) medication
(1) first line: SSRI or SNRI (see Table 18-1); if ineffective, try a second
med before trying second-line med
(2) second line: TCA (imipramine: see Table 18-1) or benzodiazepine or
buspirone (see Table 18-2). If using buspirone, increase dose q2wk
until maximum (safer than benzodiazepines).
(3) consider propranolol 10 mg or vistaril (Atarax) 10 mg before anxiety-
producing events
(4) gabapentin can help with anxiety (300 mg tid and titrate as needed);
caution about possible dizziness for 1 to 2 weeks, especially with head
position changes

647
(5) with insomnia due to “mind racing,” try imipramine, clomipramine,
or amitriptyline at hs
c) discourage ETOH and drug use (i.e., marijuana, illegal drugs) to help
with anxiety; these can cause rebound anxiety, worsen any depression,
and lead to addiction problems
d) if GAD is not controlled, refer to a psychologist, psychiatrist, or
psychiatric NP for management
B. Panic disorder
1. Diagnosis
a) discrete episodes of sudden-onset intense fear lasting minutes to an
hour
b) often associated with
(1) chest pain, palpitations, tachycardia
(2) shortness of breath, choking sensation
(3) dizziness, trembling, or shaking
(4) fear of “going crazy” or of dying
2. Treatment
a) first line: cognitive behavioral therapy
b) often also given SSRI or SNRI (see Table 18-1); paroxetine or
venlafaxine are commonly used
c) consider benzodiazepine for the first few weeks until SSRI starts
working (see Table 18-2); taper benzodiazepine 10% per week to limit
withdrawal symptoms and recurrent panic
d) if not controlled, refer to a psychiatrist or psychiatric NP for
management
C. PTSD
1. Description: results from the complex effects of psychological trauma
(e.g., military combat, natural disasters, rape, abusive situations); it is
characterized by recurrent thoughts, nightmares and flashbacks;
avoiding reminders of the trauma; hypervigilance and sleep
disturbances
2. Treatment: If considering this condition, refer to a psychiatrist or

648
 psychiatric NP because of the difficulty in diagnosis and complexity in
management
IV. Extrapyramidal symptoms (EPS)

A. Description: abnormal movements associated with the use of

antipsychotic med, especially neuroleptics (see Table 18-3); patients
with EPS may be at higher risk for developing tardive dyskinesia (see
next page)
B. Acute onset very soon after starting med (versus tardive dyskinesia,
which occurs months or more after starting med)
C. Types of extrapyramidal symptoms (EPS)
1. Akathisia (most common EPS)
a) symptoms: feeling of motor restlessness, accompanied by an inability
to sit or stand still (e.g., repeated leg crossing, weight shifting)
b) treatment
(1) cautious decrease in the dose of the offending med
(2) if inadequate, try benzodiazepines or propranolol
2. Parkinsonism (not related to Parkinson’s disease)
a) symptoms: masklike faces, drooling, resting tremors, cogwheel
rigidity, or shuffling gait
b) treatment
(1) if uncomfortable or disabling, control with benztropine for a few
weeks to 2 to 3 months; then, reevaluate if the patient requires further
treatment
(2) occasional dose reduction or antipsychotic med discontinuation is
needed
3. Dystonias
a) symptoms: involuntary contractions of major muscle groups (e.g.,
torticollis, retrocollis, opisthotonos, oculogyric crisis, tonic spasm of
masticatory muscles)
b) treatment
(1) symptoms have a rapid onset and are very disturbing to patients

649
 (2) may use benztropine 1 to 2 mg PO or diphenhydramine 50 mg IM or
IV
(3) refer or transfer to ED immediately
D. Evaluation for EPS
1. Evaluate when starting an antipsychotic med, weekly until med dose
has been stable for ≥2 weeks, and then at least q6mo thereafter
2. Use the same format each time for consistency; a commonly used test
is the Abnormal Involuntary Movement Scale (AIMS) found at
www.cqaimh.org/pdf/tool_aims.pdf
3. There is no “right” score; comparison of scores provides information
on the development of involuntary movements (i.e., tardive
dyskinesia: see next section)
V. Tardive dyskinesia (TD)

A. Description: characteristic involuntary movements that appear after

≥1 month on a neuroleptic med (see Table 18-3) or metoclopramide;
symptoms commonly appear after decreasing the dose or changing to
a less potent med or after the med is stopped
B. Onset is often insidious. Symptoms include sucking or smacking lips,
facial grimacing, lateral jaw movements, protruding and twisting
movements of the tongue, torticollis, and choreoathetoid movements
(i.e., rapid, purposeless, spontaneous) of the extremities or trunk.
C. Patients on antipsychotic meds should be evaluated at least q6mo (see
AIMS, under Evaluation for EPS above); patient with EPS during acute
treatment may be at greater risk for TD
D. Treatment
1. There is currently no medication effective for treating TD
2. Change to an atypical antipsychotic (low risk for TD); remission of TD
may occur after several months off the offending med, but often is
irreversible, despite stopping the med
3. Consider referral to a psychiatrist or psychiatric NP
Table 18-2
Anxiolytics

Drug Dosage Range (mg qd) Half-life of the Parent Drug (h)

650
 Benzodiazepines*
Alprazolam (Xanax) General: 0.25-4 12-15
Panic: 1.5-10
Chlordiazepoxide (Librium, Mitran) 5-100 30-100
Clonazepam (Klonopin) 1.5-4 18-50
Clorazepate (Tranxene) 7.5-60 36-200
Diazepam (Valium, Zetran) 4-40 50-100
Lorazepam (Ativan) 0.5-6 10-14
Oxazepam (Serax) 30-120 5-15
Miscellaneous
Buspirone (BuSpar) 15-60 (not for prn use) 48-72
Hydroxyzine (Atarax, Vistaril, others) 50-400 n/a
*Benzodiazepines
have the potential for addiction.

Table 18-3
Common Antipsychotic Agents

Dosage Range Extrapyramidal Orthostatic Anticholinergic

Drug Sedation
(Adult; mg qd) Side Effects Hypotension Effects
First Generation (Neuroleptics or Conventional Antipsychotics)
Chlorpromazine 30-800 +++ ++ +++ ++
(Thorazine)
Fluphenazine 1-40 + ++++ + +
(Prolixin)
Haloperidol 2-100 IM 0/+ ++++ + +
(Haldol)
Thioridazine 150-800 +++ + +++ +++
(Mellaril)
Second Generation (Atypical Antipsychotics)*
Aripiprazole 2-30 + 0 + 0/+
(Abilify)
Clozapine† 12.5-900 +++ 0 +++ +++
(Clozaril) (usually 100-
150)
Olanzapine 5-20 ++ + ++ ++
(Zyprexa)
Paliperidone 3-12 + 0/+
(Invega)
Quetiapine 50-800 ++ 0 ++ 0/+
(Seroquel)
Risperidone 4-16 + ++ ++ 0/+
(Risperdal)
Ziprasidone 40-200 ++ ++ ++ +
(Geodon)
*
Many of these meds can cause weight gain, DM (monitor FBG levels at least yearly), and hyperlipidemia (monitor periodically).
†Monitor WBC count with differential weekly while the patient is undergoing therapy and for 4 weeks after discontinuation.
0, none; +, slight; ++, moderate; +++, high.

651
Cognitive impairment
I. Description

A. “Normal” aging: mainly mild changes in memory and rate of

processing new information, but these are not progressive and do not
affect daily function
B. With mild cognitive impairment and dementia: memory impairment
is the primary complaint; other cognitive or behavior changes may also
be present
II. Evaluation

A. The initial appointment should focus on the history; ideally, a family

member is also present to give a history of cognitive and behavioral
changes because the patient may not think there is anything wrong or
notice any problems
B. Medication history (prescription and OTC) is very important, as many
drugs can cause mental status changes
C. Complete physical examination, including neurological examination
D. Cognitive function
1. Clock drawing test: screening to differentiate normal elderly aging
from dementia (see Box 18-1)
2. Mental status examination (see Box 3-1)
E. To rule out reversible causes of dementia
1. Lab tests: CBC, ESR, vitamin B12 and folic acid levels, TSH and free T4,
chemistry panel, and serum ammonia
2. Consider RPR or VDRL (neurosyphilis), HIV (as indicated)
3. Probable CT or MRI of the brain (subdural hematoma, brain tumor,
cryptococcus); see Table 4-2
4. Carotid Doppler studies; possibly echocardiogram
F. Consider early referral for formal neuropsychological testing (can
detect cognitive changes of various types of dementia)
III. Mild cognitive impairment (MCI)

652
 A. Description: memory difficulties but able to function in daily life;
there is increased risk for dementia
B. Symptoms
1. Impaired memory (primary complaint), which is upsetting to the
patient
2. May also have depression, anxiety, irritability, apathy
3. NO problems with ADLs
4. Mild problems with word skills (e.g., “word search”), which is
upsetting to the patient
C. Evaluation is used to establish the severity of impairment and provide
a baseline
1. The criteria are not precise; it may be difficult to determine what is
normal impairment for the patient or what may indicate dementia
2. See Evaluation section on previous page.
D. Treatment
1. No pharmacologic treatment has been shown to help memory or
lessen the chance of developing dementia
2. Screen for and treat vascular risk factors (e.g., HTN, DM, lipids,
smoking)
3. Consider referral for formal neuropsychological testing
4. Diagnosis of MCI can help the patient and family be proactive in
decisions about the future
IV. Dementia

A. Description: chronic progressive memory problems, especially with

learning new things, plus impairment with at least 1 of the following:
1. Handling complex tasks (e.g., balancing checkbook)
2. Reasoning (e.g., difficulty coping with unexpected events)
3. Spatial ability/orientation (e.g., getting lost in familiar places)
4. Executive functioning: decision-making abilities and the ability to
carry out plans
5. Speaking clearly

653
B. It does eventually affect ADLs
C. Most common types: Alzheimer’s disease (AD), vascular dementia,
dementia with Lewy bodies, and Parkinson’s disease with dementia. It
also results from chronic alcoholism or repeated head injuries (e.g.,
professional boxers).
D. Dementia must be distinguished from delirium and depression (see
Table 18-4)
E. Treatment
1. If changes occur within 6 months (e.g., independent 6 to 12 months ago and
now needs help): urgent referral to a specialist (possible causes: vascular
disease, Hashimoto’s thyroiditis, Creutzfeldt-Jakob disease, CA,
vasculitis, cerebral infection)
2. Follow-up in office to monitor the patient’s physical abilities and
caregiver’s coping ability at least q6mo; repeat cognitive testing q1yr
(see Evaluation, Cognitive Impairment). Encourage end-of-life
planning (including appointing a POA for health care) while the
patient still has some cognitive function for decision making.
3. Medications
a) cholinesterase inhibitors: donepezil (Aricept), rivastigmine (Exelon,
oral and patch), galantamine (Razadyne, Razadyne ER): used with AD,
vascular dementia, dementia with Lewy bodies, or Parkinson disease
b) memantine (Namenda): used with mod-to-severe AD and vascular
dementia; little benefit with mild AD
c) the following have shown no benefit: NSAIDs, estrogen, vitamin E or
B, Ginkgo biloba, statins, omega-3 fatty acids
4. Encourage mental exercises such as crosswords, word-finding games,
and puzzles
5. Behavior management (behavior changes lead to increased functional
impairment)
a) minimize changes in daily routines and establish a calm nighttime
routine
b) encourage physical activity and exercise (e.g., daily walk); this helps
prevent physical decline and improves behavior problems

654
 c) with delusions/hallucinations
(1) no treatment if not disturbing to the patient or family
(2) use antipsychotics (see Table 18-3) only for disturbing symptoms or
dangerous behaviors
d) with depression or agitation: consider citalopram 20 mg qd or
trazodone hs
e) sleep disorder: nonpharmacologic strategies preferred (e.g., activity
program, no daytime naps, avoid evening alcohol and caffeine)
6. Safety issues
a) ensure a safe environment (e.g., turn water heater to ≤120°F, provide
good lighting and night lights, “unclutter” the house and do not move
furniture, install grab bars in the bathroom). If needed, install stove
cut-off switch and lock up matches and firearms.
b) place locks on windows and doors (all people with dementia are at
risk of wandering and becoming lost)
c) discourage driving
7. Miscellaneous
a) use memory aids and cues (e.g., handwritten daily schedule, labeling
rooms and drawer contents, medication organizers)
b) continued involvement in social activities (e.g., church, senior citizen
activities) as long as possible is important
c) inability to handle finances is inevitable with all patients; this should
be addressed with the patient and family early after diagnosis
d) when independent living is no longer safe, options other than nursing
home placement include live-in assistance (family or hired caregivers),
adult daycare, respite, or residential care
Table 18-4
Disorders of Cognition

Disorders Symptoms
Dementia Insidious onset; slowly progressive
Impairment of memory
More common in elderly

Delirium Abrupt onset

655
 Inattention and clouding of the sensorium
Perceptual disturbances, hallucinations
Anxiety, drowsiness

Depression Variable onset

Normal memory but may have poor attention
No hallucinations
May have anxiety, hopelessness

Box 18-1

C l o c k Te s t
The clock test is used to differentiate normal elderly aging from dementia.
Instructions

Ask the patient to draw a clock and put numbers in their correct positions. Have the patient
draw hands indicating:

• 10 minutes after 11
OR
• 20 minutes after 8
Scoring

Patient receives 1 point for each of these criteria:

• Draws closed circle

• Places numbers in sequence
• Correct spatial arrangement
• Includes clock hands
• Places hands in the correct position
Results

Any score <5 indicates the need for further evaluation.

656
APPENDIX A. Food sources for selected nutrients

Vitamin K Iron Potassium

Green Leafy Vegetables Meat and Meat Substitutes Cereals

Broccoli Bran flakes

Organ meats
Brussels sprouts Kellogg’s All Bran
All meats and poultry
Cabbage Nabisco 100% Bran
Egg yolk
Collard greens Shredded wheat
Shellfish
Cucumber peel Fruits
Tofu, soybeans
Endive Apricots, dates, or peaches (dried
Fruits or fresh)
Green scallions
Apricots, prunes Avocado
Kale
Grapes Banana
Lettuce
Raisins Cantaloupe
Mustard greens
Vegetables Orange, grapefruit, or tomato
Parsley (fruit or juice)
Broccoli
Spinach Prunes and raisins
Brussels sprouts
Turnip greens Watermelon
Collard greens
Vegetables
Watercress
Celery
Fats Asparagus
Green leafy vegetables
Canola, salad, soybean, and Baked potato or sweet potato
olive oils Lettuce
Baked winter squash
Mayonnaise Miscellaneous

657
 Beet greens
Margarine Dried peas, beans
Broccoli
Miscellaneous Fortified cereals, including
baby cereals
Carrots
Beans
Grains, legumes Chard
Pickles
Potatoes
Lima beans
Sauerkraut
Mushrooms
Soybeans
Peas, cooked

Spinach, fresh

Miscellaneous

Blackstrap molasses

Canned tomato sauce

Chocolate, unsweetened

Cooked white beans

Peanuts

Sardines, canned in oil

Sunflower seeds

Folic Acid Sodium Calcium

Green Leafy Foods to Avoid on a Sodium-Restricted Diet: Dairy Products
Vegetables (providing ≥200
Milk and Dairy Products mg/serving)
Asparagus
Buttermilk, malted milk Cheese: hard cheese,
ricotta, or cottage
Broccoli
cheese
Many cheeses
Cereals
Ice cream

658
 Meat and Meat Substitutes
Oatmeal Milk (whole, 2%, or
Any meat, fish, poultry that is smoked, cured, salted, or skim)
Wheat bran canned (e.g., bacon, dried beef, cold cuts, ham/turkey
ham, hot dogs, sausages) Milk shakes
Miscellaneous
Bread and Grains Yogurt
Bananas
Bread/rolls/crackers with salted tops Meat and Meat
Fish Substitutes
Quick breads
Liver (providing ≥100
Instant hot cereals mg/serving)

Peanut butter
Pancakes, waffles, muffins, biscuits, and corn bread Clams

Red beans with salt, baking powder, or self-rising flour or as

instant mixes Oysters

Regular bread crumbs, cracker crumbs Sardines and salmon

(with bone)
Instant rice and pasta mixes
Shrimp
Stuffing and casserole mixes
Tofu
Vegetables and Fruits
Vegetables and
Frozen vegetables in sauce Fruits

Regular canned vegetables, juices (providing ≥90

mg/serving)

Sauerkraut, pickled vegetables

Broccoli

Pickles, olives
Kale, turnip greens

Miscellaneous
Okra

Regular catsup, chili sauce, mustard, horseradish,

sauces: BBQ, soy, teriyaki, Worcestershire, and steak Orange juice (calcium
fortified)

Regular canned or dried soup, bouillon

Spinach

Salt in seasonings (e.g., garlic salt)

659
 Breads, Grains,
Seasonings containing MSG Legumes (providing
≥90 mg/serving)
Salted snack foods (e.g., chips, nuts, pretzels, seeds,
popcorn) Beans

English muffin

Fortified, ready-to-eat
cereal

Fortified bread

Waffles
BRATY Diet
The BRATY diet can be used for patients with nausea and vomiting. The food consistency depends on the age of the patient and
personal preference; e.g., bananas can be fresh, mashed, or from baby food jar. The diet can be used up to 24 h.
B: bananas
R: rice or rice cereal
A: apples, applesauce
T: toast, crackers (preferably dry)
Y: yogurt, live culture (preferably plain)

660
Index
Page numbers followed by f indicate figures; t, tables; b, boxes.
A
Abdomen
focused examination of, 20–21
palpation of, 41
pediatric assessment of, 40–41
physical examination of, 9
Abdominal disorders, 220–252
appendicitis, 238
celiac sprue, 239
in children, 410–413
cholecystitis, 232
colon cancer, 238–239
Crohn’s disease, 240
diarrhea, 241–246
differential diagnosis of, 221f, 222t
diverticulitis, 237–238
gastroenteritis, 233, 234t
gastroesophageal reflux disease, 226–229
Helicobacter pylori-induced gastritis, 231–232
hepatitis, 246–249
irritable bowel syndrome, 235–237
pancreatitis, 233–235
peptic ulcer disease, 230–231
ulcerative colitis, 240–241
Abdominal pain
differential diagnosis of, 221f, 222t
in elderly, 54–55b
Abducens nerve, 15–16t, 44

661
Abrasions, 108
Abscess, incision and drainage of, 111–112, 112t
Abstract thinking, 12
Acanthosis nigricans, 105
Accessory nerve, 15–16t, 44
Acetaminophen
for fever in children, 397, 398t
for pain, 355
Acne, 86–89
papular, 1f
pustular, 1f
treatment of, 87–88
variants of, 88
Acoustic nerve, 15–16t, 44
Actinic keratosis, 7f, 106
Activities of daily living, 62, 62–63t, 64–65t
“Acute abdomen,” 223–224
Acute arterial occlusion, 194–195
Acute bacterial rhinosinusitis, 404–405
Acute coronary syndrome, 160
Acute limb ischemia, 194–195
Acute myocardial infarction, 163–164t
Acute otitis media, 400–402
Acute pain, 352
Acute uncomplicated cystitis, 290–291
Addison’s disease, 362–363
Adie’s pupil, 14t
Adnexa, 10
Adolescents
assessment of. See Pediatric assessment
diabetes mellitus type 2 in, 386–387
growth and development of, 34t
Adrenal disorders, 362–363
Adrenal insufficiency
acute (crisis), 362
chronic, 362–363

662
Affect, 12
Agraphia, 12
Akathisia, 435
Alanine aminotransferase, 71
Albumin/creatinine ratio, 68
Alexia, 12
Allergens, 131-132. See also Asthma
Allergic contact dermatitis, 2f
Amenorrhea, 267–270
primary, 267
secondary, 267–270, 269f
Amino acids, 24
Amitriptyline, 427t, 429
Amylase, 73
Anemia, 209–219
autoimmune hemolytic, 218–219
blood loss as cause of, 212–213b, 213–214
of chronic disease, 214–215
inadequate production as cause of, 214–217
iron deficiency, 213–214, 251, 419–420
overdestruction as cause of, 217–219
pernicious, 215–216
sickle cell, 218
thalassemia, 217–218
Angina, 159–160, 162b
classification of, 159t
Animal bites, 112, 113–114
Ankle-brachial index, 197, 197t
Ankle disorders, 338–341, 340–341t
Anorexia in elderly, 54–55b
Antibiotics for acne, 87, 88t
Anticoagulation therapy, 200–205, 201t, 204–205t
Antidepressants, 427t
for pain, 356
withdrawal from, 430
Antihistamines for atopic dermatitis, 79

663
Antihypertensive agents, 182t, 183–185t, 185–187t
cautions/contraindications, 185–187t
dosing guidelines for, 183–185t
Antinuclear antibody, 74
Antipsychotic agents, 436t
Anxiety disorders, 432–436
treatment of, 433, 434, 434t, 435–436
Anxiolytics, 434, 434t
Aortic dissection, 163–164t
Aortic stenosis, 156–157t
Aphasia, 13t
Apnea, obstructive sleep, 138–139, 139b
Appendicitis, 238
Argyll Robertson pupil, 14t
Arms, 42
Arterial disease, peripheral, 194–198
Arterial occlusion, acute, 194–195
Arteritis, temporal, 315
Arthralgias, 74–75
Aspartate aminotransferase, 71
Aspirin, 397
Asthma, 126–131, 127–129t
Ataxia, 15
Atopic dermatitis, 2f, 77–79
Atrial fibrillation, 170–172
Atrioventricular block, 172–173
Attention deficit disorder, 422–423
Attention-deficit hyperactivity disorder, 422–423
Auscultation
of bowel sounds, 9
of chest, 4, 6f, 7–8
Autoimmune hemolytic anemia, 218–219
B
Babinski’s sign, 45t
Back pain, 331–334, 333t
Bacterial conjunctivitis, 142

664
Bacterial meningitis, 317
Bacterial vaginitis, 277–278
Balance assessments, in elderly, 62–63t, 63–64
Bariatric surgery, 251–252
Barlow-Ortolani test, 43
Basal cell carcinoma, 7f, 107
Bed bugs, 118–119
Bee stings, 121
Bell’s palsy, 318
Benign paroxysmal positional vertigo, 307–308b
Benign prostatic hypertrophy, 301
Benzodiazepines for anxiety, 434t
Beta blockers, 161t
Biguanides, 380
Bile acid sequestrants, 176, 177b
Biliary colic, 164
Biliary enzymes, 71
Bilirubin, in urine, 71, 72f
Bipolar disorder, 432
Birth control. See Contraception; See Contraceptives, oral
Birth history, 27
Bites, 112–114
animal, 112, 113–114
human, 108–109
insect, 114–118
Bitter orange, 24
Black cohosh for menopausal symptoms, 272
Bladder cancer, 293
Bleeding
subconjunctival, 144
uterine, 264–265
Blepharitis, 145
Blood disorders. See Vascular/blood disorders
Blood glucose
DM excursions of, adjustments for, 374–375t
self-monitoring of, 373–374, 374–375t, 376

665
Blood loss, anemia caused by, 212–213b, 213–214
Blood pressure. See also Hypertension
in children, 35t
in elderly, 53b
postural changes that affect, 2, 3
Blood urea nitrogen, 73
Bone spurs, 340
Bowel, atonic, 54–55b
Bowel sounds, 9, 41
Bowlegs, 43
Brachial pulse, 8f
Bradycardia, sinus, 172–173
Breasts
disorders affecting, 274–276
inspection of, 7
lymph nodes of, 7
masses of, 276
palpation of, 7
Tanner’s sexual maturity rating, 32–33b
Breath sounds, 39
Broca’s aphasia, 13t
Bronchial breath sounds, 6f
Bronchitis, acute, 135
Bronchovesicular breath sounds, 6f
Brudzinski’s sign, 317
Bruits, 8, 41
Bulimia in elderly, 54–55b
BUN. See Blood urea nitrogen
Bupropion, 427t, 429
Burns, 108b
“Burr cells, ” 67
Bursitis, olecranon, 328t
C
C-reactive protein, 74
Caffeine, 24
Calcium channel blockers, 161t

666
Calcium supplements, 344
Campylobacter jejuni, acute diarrhea due to, 242
Candida dermatitis, 2f
Candidiasis, vulvovaginal, 278–279
Carbuncle, 94–95, 95t, 111
Cardiac enzymes, 73
Cardiovascular assessment in elderly, 53, 53–54t
Cardiovascular disorders, 155–190
ambulatory dysrhythmias, 170–173
angina, 159–160, 162b
chest pain, 161t, 162b, 163–164t
congestive heart failure, 165–170
coronary heart disease, 158–162
endocarditis, 189–190, 190t
heart murmurs, 155–158, 156–157t, 158b
hyperlipidemias, 175t, 176t
hypertension, 178–188, 178t, 182t, 183–185t, 185–187t
metabolic syndrome, 188–189
Cardiovascular system
focused examination of, 19–20
physical examination of, 7–9, 7f, 8f
Carnett’s sign, 224
Carotid bruit versus heart murmur, 158b
Carotid Doppler ultrasonography, 75
Carotid pulse, 8f
Carotid sinus hypersensitivity, 307
Carpal tunnel syndrome, 329–330
Celiac sprue, 239
Cellulitis, 4f, 92–93, 93t
Central nervous system
infections of, 317
lesions of, 18, 18t
Cervix, 10, 11f
Chalazion, 146
Chemistries, 72–73
Chest

667
 auscultation of, 4, 6f, 7–8
pediatric assessment of, 39
physical examination of, 7–9
Chest pain, 161t, 162b, 163-164t. See also Angina
differential diagnosis of, 163–164t
in elderly, 53b
Chest radiograph, 75
Chickenpox, 100–101
Chief complaint
in adults, 1
in children, 25
Child abuse, 35, 46–47
Children. See also Pediatric disorders
assessment of. See Pediatric assessment
depression in, 431
developmental milestones in, 28–29t
diabetes mellitus type 2 in, 386–387
growth and development stages, 34t
headache in, 312
iron replacement therapy for, 420
peak expiratory flow rate in, 124–125t
vital signs in, 35t
Chlamydia infection, 282–283
Cholecystitis, 232
Cholesterol, 173
Chondromalacia patellae, 418–419
Chronic arterial occlusive disease, 195–196
Chronic disease, anemia of, 214–215
Chronic kidney disease, 298–300
Chronic obstructive pulmonary disease, 51, 73, 132–133, 134t
Chronic pain, 353–354
Chronic venous insufficiency, 192–193
Chronic wound care, 205–209
Cirrhosis, liver, 250–251
Clock test, 437b
Clonus reflex, 45t

668
Clostridium botulinum, acute diarrhea due to, 242–243
Clostridium difficile, diarrhea due to, 245–246
Clubfoot, 418
Cluster headache, 312–313
Coenzyme Q10, 177
Cognitive impairment, 437–440, 437b
Cognitive status, 12, 59b
assessing, 61b
Cognitive therapy for depression, 428
Colitis, ulcerative, 240–241
Colon cancer, 225, 238–239
Common cold, 404
Community-acquired pneumonia, 135–137, 409–410
Compression stockings, 198–199
Computed tomography, 75, 75t
Concussions, 22–23
Condoms, male/female, 254
Conductive hearing disorder, 3
Condylomata acuminata, 285–286
Congestive heart failure, 165–170, 171t
classification of, 169
medications for, 171t
testing for, 169t
Conjunctivitis, 142
allergic, 143
bacterial, 142
viral, 143
Constipation, 225–226b
Contact dermatitis, 2f, 79–80
Contraception, 254–261, 260t
barrier methods of, 254
emergency, 260–261, 260t
methods for, 254–261
Contraceptive patches, 257
Contraceptives, oral, 256, 257–261, 258–259t
Contrast medium, 75

669
Coordination, 17
Corneal abrasions, 143–144
Corneal ulcer, 144
Coronary artery insufficiency, acute, 163
Coronary heart disease, 158–162
Costovertebral angle tenderness, 9
Cough, 139b
Coumadin, 200–205, 201t, 204–205t
Crackles, 51b
Cranial nerve examination, 15, 15–16t, 44
Creatine, 24
Crepitus, knee, 335, 337–338t
Crohn’s disease, 240
Croup, 407–408
Cryptorchidism, 413
Cullen’s sign, 224
Cushing’s syndrome, 363
Cystitis
acute uncomplicated, 290–291
interstitial, 288–290
Cystocele, 288
Cysts, epidermoid, 106
D
Dacryocystitis, 145–146
DASH diet, 181t
DDP-4 inhibitors, 381
Debridement, 208
Deep tendon reflexes, 17–18, 17t
Deep vein thrombosis, 191–192
Dehydration, 396–397t
Dehydroepiandrosterone, 24
Dementia, 438–440
Dental chart, 30, 31f
Depression, 425–431
in elderly, 60
major, 428–430

670
 in pediatric patients, 431
Dermatitis
atopic, 2f, 77–79
Candida, 2f
contact, 2f, 79–80
diaper, 2f, 82
seborrheic, 1f, 83
stasis, 193–194
Dermatomes, 321f
Desyrel. See Trazodone
Development
milestones of, 28–29t
stages of, 34t
Developmental dysplasia of the hip, 417–418
DHEA. See Dehydroepiandrosterone
Diabetes mellitus, 364–370, 365t, 371–372, 373–394
blood glucose self-monitoring in, 366, 373–374, 374–375t, 376
categories of, 364
chronic complications of, 391–393
diagnosis of, 366, 366t
dietary recommendations for, 369–370, 390b
exercise and, 371–372, 372t, 373t
follow-up evaluations of, 376
foot care in, 368f, 393–394
glycosylated hemoglobin for assessing, 374–376
insulin therapy for, 377, 382–386, 383t
management goals for, 367–369
office evaluation of, 366–367
oral hypoglycemic agents for, 378, 378t, 379
screening for, 364–366
sick day management guidelines in, 389–391, 390b
symptoms of, 58b
type 1
definition of, 364
medical attention indicated in, 390–391
type 2 versus, 365t

671
 type 2
in adolescents, 386–387
in children, 386–387
definition of, 364
therapy for, 371f
Diabetic ketoacidosis, 388–389
Diagnostic tests
for arthralgias, 74–75
chemistries, 72–73
computed tomography, 75, 75t
general overview of, 66
hematology, 66–68
liver, 71–72
magnetic resonance imaging, 75, 75t
radiology, 75
urine, 68, 69–70t
Diaper dermatitis, 2f, 82
Diarrhea, 241–246
Diastasis recti, 40
Diastolic murmurs, 157
Diet
cardiovascular disease and, 162b
DASH, 181t
in diabetes mellitus, 369–370
on diabetic sick days, 390b
in hyperlipidemia, 174
for osteoporosis prevention, 344
Dimethylamylamine, 24
Discharge
from breasts, 274–275
from nipple, 274–275
Diverticulitis, 237–238
Dizziness, 307–308b
Dorsalis pedis pulse, 8f
Drawer tests, 337, 338
Dressings, occlusive, with topical steroids, 85

672
Dry eye, 145
Dumping syndrome, 251
Dysconjugate gaze, 14t
Dysmenorrhea, 263
Dysrhythmias, ambulatory, 170–173
Dysthymic disorder, 425
Dystonias, 435
E
Ear disorders
otitis media, 148, 149
tinnitus, 146–147
Ear examination
in adults, 3
in children, 36–38, 37f
Eczema, 77–79
Edema, 53b
Effexor. See Venlafaxine
Ehrlichiosis, 115–116
Elavil. See Amitriptyline
Elbow
dislocation of, 328t
disorders affecting, 327–328, 328t
range of motion test for, 327f
Elderly, assessment of. See Geriatric assessment
Electrocardiogram, 165, 166f
Elevated arm stress test, 326
Embolism, pulmonary, 163
Emotional abuse, 46–47
Encopresis, 411–412
Endocarditis, antibiotic prophylaxis against, 189–190, 190t
Endocrine assessment in elderly, 58, 58–59t
Endocrine disorders, 359–394
adrenal, 362–363
diabetes complications, 391–394
diabetes mellitus, 364–370, 365t, 371–372, 373–394
hyperglycemia, 389–391

673
 thyroid, 359–361, 361t
Enteritis, regional, 240
Enuresis, 413–414
Epicondylitis, 328t
Epidermal inclusion cyst, 1f
Epidermoid cysts, 106
Epididymitis, 302
Epiglottitis in children, 408–409
Episodic illness examination, 26–27
Epistaxis, 149
Epstein-Barr virus, 152
Equilibrium disturbances, 305–308, 307–308b
Erb’s point, 7f
Erectile dysfunction, 303–304
Erysipelas, 91–92, 92t
Erythema infectiosum, 6f, 97
Erythrocyte sedimentation rate, 74
Esophageal spasm, 164
Esophagitis, 164
Evening primrose oil for menopausal symptoms, 272
Examination. See also Physical examination
focused. See Focused examination
routine well-woman, 21
Exercise
for diabetic patient, 371–372, 372t, 373t
food and insulin adjustments for, in DM, 373t
Extrapyramidal symptoms, 434–435
evaluation for, 435
Eye disorders, 142–146
Eye examination
in adults, 3, 14t
in children, 36
ophthalmologic, 13t, 14t
F
Facial nerve, 15–16t, 44
Failure to thrive, 400

674
Falls, 55–56, 56t, 62–63t, 63–64, 64–65t
Family history
in adults, 2
in children, 30
Fatigue, 320t
Feet. See Foot
Femoral pulse, 8f, 40
FEV1, 123, 125t
FEV1/FVC ratio, 123, 125t
Fever
in infants/children, 395–397
management of, 398t, 399t
Fever blisters, 98–99
Fibric acid derivatives for hyperlipidemias, 176
Fibrocystic breast disease, 276
Fibromyalgia, 347–350
diagnosis of, 347–349
tender points for, 348f
treatment of, 349–350
Fifth’s disease, 6f, 97
Finger-to-nose test, 17
Fire ant stings, 121–122
Flaxseed, 177
Flexural atopic dermatitis, 2f
Fluent aphasia, 13t
Fluoxetine, 427t, 428–429
Focal neurological deficit, 317–318
Focused examination
of abdominal system, 20–21
of cardiovascular system, 19–20
of respiratory system, 18–19
Folate deficiency, 216, 252
Folliculitis, 3f, 93–94, 94t
Fontanelles, 36
Foods, latex cross-reaction with, 80t
Foot

675
 anatomy of, 339f
care of, in diabetic patients, 368f, 393–394
disorders of, 338–341, 340–341t
lateral ligaments of, 340f
medial ligaments of, 340f
Forced vital capacity, 123, 125t
Functional assessment of elderly, 62, 62–63t, 64–65t
Fungal infections of skin, 101–103
Furuncle, 94–95, 95t, 111
G
Gait
assessment of
in adults, 12, 15, 17
in children, 42
in elderly, 56b, 62–63t, 63–64
Gastritis, Helicobacter pylori-induced, 231–232
Gastroenteritis
acute, 233, 234t
in children, 410–411
Gastroesophageal reflux disease, 226–229
in children, 412–413
Gastrointestinal assessment in elderly, 54–55, 55t
General appearance, 2
Generalized anxiety disorder, 433
Genital warts, 285–286
Genitalia
female, 10, 11f, 12f
male, 9
physical examination of, 9, 10, 11f, 12f
Tanner’s sexual maturity rating, 32–33b
Genitourinary system
assessment of, in elderly, 56–57, 57t
disorders of, in children, 413–415
examination of, 41–42
Genu valgum, 43
Genu varum, 43

676
Geriatric assessment, 48
cognitive/emotional status, 60–61
comprehensive, 49–57, 58, 59
cardiovascular system, 53, 53–54t
endocrine/immune systems, 58, 58–59t
gastrointestinal system, 54–55, 55t
genitourinary system, 56–57, 57t
integumentary system, 50, 50t
musculoskeletal system, 55–56, 56t
neurologic system, 59, 60t
respiratory system, 51, 53t
sensory system, 51, 52t
for depression, 60, 61t
functional, 62, 62–63t, 64–65t
health history in, 33
for risk of falling, 62–63t, 63–64, 64–65t
Geriatric Depression Scale, 60, 61t
Gestational diabetes, 366t
Giardia lamblia, acute diarrhea due to, 243, 244
Ginseng for menopausal symptoms, 272
Glaucoma, acute closed-angle, 144
Glitazones, 381
Global aphasia, 13t
Glomerulonephritis, acute, 293
Glossopharyngeal nerve, 15–16t, 44
GLP-1 receptor agonists, 381
Glucose, blood. See Blood glucose
α-Glucosidase inhibitors, 381
Gluten intolerance enteropathy, 239
Glycosylated hemoglobin. See Hemoglobin A1c
Goiter, 359
Gonorrhea, 282
Gout, 346–347
Grey-Turner’s sign, 224
Growth and development. See Development
Guggulipid, 177

677
Guillain-Barr syndrome, 316
Gynecologic assessment
contraceptive methods, 254–261
Pap smear in, 253–254
Gynecologic conditions, 253–286
abnormal uterine bleeding, 264–265
amenorrhea, 267–270
bacterial vaginitis, 277–278
breast conditions, 274–276
contraceptive methods, 254–261, 258–259t, 260t
dysmenorrhea, 263
menopause, 270–274
Pap smear in, 253t
PMS, 261–262
polycystic ovary syndrome, 265–267
vulvar vestibulitis/vulvodynia, 277–278
H
Hand
anatomy of, 329f
disorders of, 329–331, 330t
Hand-foot-and-mouth disease, 6f, 97–98
Head
lymph nodes of, 6f
pediatric assessment of, 36
physical examination of, 3, 36
Head lice, 8f, 119, 120
Head-to-shin test, 17
Headache
in children, 312
red flag, 311–312
Health history, in pediatric assessment, 25–33, 26b
Hearing
defects of, 3
testing of, 37–38
Heart auscultation, 7f
Heart failure. See Congestive heart failure

678
Heart murmurs, 155–158, 158b
classification of, 156–157t, 157f
in elderly, 53b
Heart rate, 35t
Heart sounds, 7
in elderly, 53b
Heel pain, 340
Helicobacter pylori-induced gastritis, 231–232
Hematocrit, 67
Hematology diagnostic tests, 66–68
Hematopoietic disorders in children, 419–420
Hematuria, 287–288b
Hemoglobin, 67
Hemoglobin A1c, 73, 374–376
Hemolytic anemia, autoimmune, 218–219
Hemorrhage, subconjunctival, 144
Hemorrhoids, 226
Hepatitis, 246–249
Hepatitis A, 246–247
Hepatitis B, 247–248
Hepatitis C, 248–249
Hepatocellular enzymes, 71
Herbal preparations
in menopausal therapy, 272
pain management using, 354
Hernia, 41
Herpes genitalis, 5f, 284–285
Herpes simplex infection, 5f, 98–99
Herpes zoster infection, 5f, 99–100
Hip(s)
description of, 43
developmental dysplasia of, 417–418
disorders of, 331–334, 332–333t
Histamine blockers, 81
History, 1–18
family, 2, 30

679
 past medical, 1–2, 27
prenatal, 27
psychosocial, 2
recording of, 2
social, 30
History of the present illness
in adults, 1
in children, 25–27
Hives, 81–82
Hordeolum, 146
Hormone replacement therapy, 271t, 272
Human bites, 108–109
25-Hydroxyvitamin D, 73
Hyperesthesia, 17
Hyperhidrosis, 83
Hyperlipidemia, 173–177
medications for, 175t, 176t
Hyperosmolar hyperglycemic state, 389
Hyperresonance, 4
Hypertension, 178–188
in children, 423–424
classification of, 178t
DASH diet for, 181t
medications for, 182t, 183–185t, 185–187t
cautions/contraindications for, 185–187t
dosing guidelines for, 183–185t
treatment of, 180–188
Hyperthyroidism, 360–361
Hyphema, 144–145
Hypoglossal nerve, 15–16t, 44
Hypoglycemia
oral agents for, 378, 378t, 379
in type I DM, 387–388, 388t
Hyponatremia, 72
Hypospadias in children, 413
Hypothyroidism, 359–360

680
Hypoventilation, 74
I
Ibuprofen, for fever in children, 397, 399t
Immune assessment in elderly, 58, 58–59t
Impetigo, 3f, 90–91, 91t
Impotence, 57b, 303–304
Incision and drainage, of abscess, 111–112, 112t
Incontinence, urinary, 295–297
Infections
central nervous system, 317
ear, 148, 149
skin, 90–95
fungal, 101–103
viral, 95–101
urinary tract, 288
Infectious mononucleosis, 152
Inflammation, joint, 319t, 345–347
Inflammatory pain, 354
Influenza, 152–154
in children, 406–407
Insect bites, 114–118
Insulin, 373t
pharmacokinetics of, 383t
regimens for, 384–385
therapy with, 377, 383t
Integumentary assessment. See also Skin disorders; See also specific disorders
geriatric, 50, 50t
Intrauterine devices, 254–255
Intussusception in children, 410
Iritis, 143
Iron deficiency anemia
in children, 419–420
description of, 213–214, 251
Iron replacement therapy for children, 420
Irritable bowel syndrome, 235–237
J

681
Joints
inflammatory conditions of, 319t, 345–347
painful disorders of, 345–347
Jugular venous pressure, 8
K
Kehr’s sign, 224
Keratitis, ulcerative, 144
Keratoacanthoma, 106–107
Keratoconjunctivitis, 145
Keratosis, actinic, 7f, 106
Kernig’s sign, 317
Ketoacidosis, diabetic, 388–389
Kidney disease, chronic, 298–300
Kidney stones, 294–295
Knee
anatomy of, 336f
disorders of, 334–338, 337–338t
Knock knees, 43
L
Labial adhesions, 420–421
Lacerations, 108, 109–111
suturing of, 109–111, 110t
Language assessments, 12, 13t
Latex, products containing, 80t
Latex dermatitis, 79–80
Leg length discrepancy, 43
Legs, 43
Lesions, skin, 105–108
Leukocytosis, 66–67
Leukopenia, 67
Levonorgestrel IUD, 255
Lichen sclerosis, 104
Lichenification, flexural atopic dermatitis with, 2f
Limping, 416–417
Lipase, 73
Lipids, elevated levels of. See Hyperlipidemia

682
Lipoprotein(a), 177b
Liver
cirrhosis of, 250–251
in geriatric assessment, 55t
Liver disease, 249–250
Liver function tests, 71
Low back pain, 331–334, 333t
Lower extremity edema, 9
Lyme disease, 114–115
Lymph nodes
of breasts, 7
of head, 6f
of neck, 4, 6f, 39
palpation of, 4, 6f, 39
pediatric assessment of, 39
M
Magnetic resonance imaging, 75, 75t
Malaise, 320t
Malaria, 118
Malignant melanoma, 7f
Manic episodes, 432
Marcus Gunn pupil, 3, 14t
Markle sign, 223–224
Mastitis, 275–276
McMurray’s test, 336, 337–338t
Medication history, 30
Meglitinides, 379
Melanoma, 107–108
Melasma, 103–104
Meniere’s disease, 307–308b
Meningitis, viral/bacterial, 317
Menopause, 270–274
Menstrual migraines, 263–264
Mental status, 59b
assessing, 61b
Mental Status Questionnaire, short portable, 60, 61b

683
Metabolic syndrome, 188–189
Migraine headache, 306, 313–315, 314t
menstrual, 263–264
triggers of, 314t
Mild cognitive impairment, 438
Mirtazapine, 427t, 429
Mitral regurgitation, 156–157t
Mitral stenosis, 157
Mitral valve prolapse, 156–157t
Mixed lung diseases, 123
Molluscum contagiosum, 4f, 95–96
Monoamine oxidase inhibitors, 430
Monofilament testing sites on feet, 368f
Moro reflex, 45t
Mosquito bites, diseases due to, 117–118
Motor strength testing, 15
Mouth examination, 38
Multiple sclerosis, 316
Murmurs. See Heart murmurs
Murphy’s sign, 224
Muscle relaxers, for pain, 355
Muscle strength, 321t
Muscle weakness, 56b
Musculoskeletal assessment, in elderly, 55–56, 56t
Musculoskeletal disorders, 319–351
of ankle, 338–341, 340–341t
in children, 415–418
of elbow, 327–328, 327f
fibromyalgia, 347–350
of foot, 338–341, 340–341t
of hand, 329–331, 330t
hip/low back pain, 331–334, 333t
history-taking, 319
of joints, 345–347
of knee, 334–338, 337–338t
of neck, 320–322, 323t

684
 osteoporosis, 343–345
restless leg syndrome, 350–351
shoulder pain, 322–327, 323f, 324t, 325f
strains/sprains, 342
of wrist, 329–331, 330t
Musculoskeletal pain, 353–354
Musculoskeletal system examination
in adults, 12
in children, 42–44
Myasthenia gravis, 316–317
Myelodysplastic syndrome, 216–217
Myocardial infarction
acute, 163–164t
prevention of, 162b
N
Nailbed, capillary refill testing of, 4
Neck
disorders of, 320–322
inspection of, 8
lymph nodes of, 4, 6f, 39
pain in, 323t
pediatric assessment of, 39
range of motion in, 320
Neglect, child, 46
Neonatal history, 27
Nephropathy in DM, 391
Neuralgia, postherpetic, 99–100
Neurologic assessment, in elderly, 59, 60t
Neurologic disorders, 305–318
CNS infections, 317
equilibrium disturbances, 305–308, 307–308b
headaches, 311–316
neuromuscular disorders, 316–317
Parkinson’s disease, 310
seizures, 308, 308b, 309f
tremors, 308–310

685
Neurological deficit, focal, 317–318
Neurological system
cranial nerves, 15, 15–16t
motor examination, 15, 44
pediatric assessment of, 44–46
physical examination of, 12–18, 13t, 14t, 15–16t
sensory examination, 44–45
Neuromuscular disorders, 316–317
Neuromuscular lung diseases, 123
Neuropathic pain, 353, 356
Neuropathy, diabetic, 391–393
Niacin, 177b
Nicotinic acid for hyperlipidemias, 176
Nipple discharge, 274–275
Nitrates for angina, 161t
Nocturia, 288
in elderly, 57b
Nonalcoholic fatty liver disease, 249, 250
Nonfluent aphasia, 13t
Nonpitting edema, 9
Nonsteroidal anti-inflammatory drugs, for pain, 354–355
Norwalk-like virus, acute diarrhea due to, 243
Nose, 3
Nosebleed, 149
Nurse maid’s elbow, 328t
Nutrition. See Diet
Nystagmus, 14t
O
Obstructive lung diseases, 123
Obstructive sleep apnea, 138–139, 139b
Obturator test, 223–224
Occlusive dressings with topical steroids, 80t
Ocular disorders, 140–154
Oculomotor nerve, 15–16t, 44
Olecranon bursitis, 328t
Olfactory nerve, 15–16t, 44

686
Omega-3 fatty acids, 177
Onychomycosis, 102–103
Ophthalmologic examination, 13t, 14t
Opiates, for pain, 355–356
Optic atrophy, 13t
Optic nerve, 15–16t, 44
Oral contraceptives, 256, 257–261, 258–259t
Oropharynx examination
in adults, 4
in children, 38
Orthostatic syncope, 306
Osgood-Schlatter disease, 419
Osmolality, serum, 72
Osteoarthritis
characteristics and treatment of, 345–346
of hand/wrist, 330t
Osteoporosis, 343–345
Otitis externa
in adults, 147–148
in children, 402–403
Otitis media, 148, 149
acute, 400–402
in children, 400–402
with effusion, 402
Otoscopy, 3, 4f
Overflow incontinence, 297
P
Pain, 352–358
abdominal
differential diagnosis of, 221f, 222t
in elderly, 54–55b
acetaminophen for, 355
acute, 352
adjuvant therapies for, 356–357
anticonvulsants for, 356
antidepressants for, 356

687
 assessment of, 352–357
chest. See Chest pain
chronic, 353–354
elbow, 327–328
herbal preparations for, 354
inflammatory, 354
joint, 345–347
knee, 334–338, 337–338t
low back/hip, 331–334, 333t
muscle relaxers for, 355
musculoskeletal, 353–354
neck, 323t
neuropathic, 353, 356
nonpharmacologic therapies for, 354
nonsteroidal anti-inflammatory drugs for, 354–355
ocular, 141
opiates for, 355–356
pharmacologic therapies for, 354, 357b
rating scales for, 352
shoulder, 322–327, 324t
therapies for, 354–357, 357b
visceral, 220, 354
Palmar grasp reflex, 45t
Pancreatitis, 73, 233–235
acute, 164
Panic disorder, 433–434
Pap smear, 10
abnormal, 254
managing results of, 253t
Papilledema, 13t
Parachute response reflex, 45t
Parasitic infestation, 118–121
Paresthesia, 17
Parietal pain, 220
Parkinsonism, 435
Parkinson’s disease, idiopathic, 310

688
Paroxetine, 427t
Paroxysmal supraventricular tachycardia, 172
Past medical history
in adults, 1–2
in children, 27
Patellofemoral pain syndrome, 418–419
Paxil. See Paroxetine
Peak expiratory flow rate, 123
Pediatric assessment. See also Children
approach to, 25
child abuse, 35, 46–47
comprehensive, 33–46
developmental milestones, 28–29t
general observations, 33–35
goals of, 25
growth and development stages, 34t
health history, 25–33, 26b
Pediatric disorders, 395–424
abdominal, 410–412
allergic rhinitis, 403–404
attention-deficit hyperactivity disorder, 422–423
bronchiolitis/croup, 407–410
common cold, 404
congenital talipes equinovarus, 418
cryptorchidism, 413
dehydration, 396–397t
developmental dysplasia of the hip, 417–418
encopresis, 411–412
enuresis, 413–414
epiglottitis, 408–409
failure to thrive, 400
fever, 395–397, 398t, 399t
gastroenteritis, 410–411
gastroesophageal reflux disease, 412–413
genitourinary, 413–415
hematopoietic, 419–420

689
 hypertension, 423–424
hypospadias, 413
influenza, 406–407
intussusception, 410
iron deficiency anemia, 419–420
labial adhesions, 420–421
limping, 416–417
lower respiratory, 407–410
musculoskeletal, 415–418
Osgood-Schlatter disease, 419
otitis externa, 402–403
otitis media, 400–402
patellofemoral pain syndrome, 418–419
pharyngitis, 405–406
pneumonia, 409–410
pyloric stenosis, 410
respiratory syncytial virus, 409
scoliosis, 415–416
sinusitis, 404–405
upper respiratory, 400–407
urinary tract infection, 414–415
vulvovaginitis, 421–422
Pediculosis capitis, 119, 120
Pelvic inflammatory disease, 280–281
Peptic ulcer disease, 164, 230–231
Pericarditis, 163–164t
Peripheral arterial disease, 194–198
exercise program for, 197–198
Peripheral nervous system lesions, 18, 18t
Peripheral neuropathy in elderly, 59b
Peripheral pulses, 8, 8f
Peripheral vascular disease, chronic, 191–205
Peripheral venous disease, 191–194
chronic venous insufficiency, 192–193
deep vein thrombosis, 191–192
stasis dermatitis, 193–194

690
 superficial thrombophlebitis, 192
Pernicious anemia, 215–216
Personal history, 30
Pes planus, 43
Pharyngitis, 151–152
in children, 405–406
Pheochromocytoma, 363
Photophobia, 141
Physical abuse, 46, 47
Physical examination
abdomen, 9
cardiovascular system, 7–9, 7f, 8f
cervix, 10, 11f
chest, 7–9
ears, 3
eyes, 3
general appearance, 2
genitalia, 9, 10, 11f, 12f
guideline for, 1–24
head, 3
history, 1–18
neurological system, 12–18, 13t, 14t, 15–16t
nose, 3
oropharynx, 4
pediatric, 35–47
respiratory system, 4, 6f
skin, 3
sports, 21–24
uterus, 10, 11f
vital signs, 2–3
Pigmentation disorders, 103–105
Pinguecula, 142
Pitting edema, 9
Plantar fasciitis, 340
Platelets, 67–68
Pneumomediastinum, 163

691
Pneumonia
in children, 409–410
community-acquired, 135–137, 409–410
diagnosis of, 164
Pneumothorax, 163
Pneumovax 23, 51
Point of maximal impulse, 40
Polycystic ovary syndrome, 265–267
Polysomnography, 138
Popliteal pulse, 8f
Posterior tibial pulse, 8f
Postherpetic neuralgia, 99–100
Posture, 2, 3
Potassium supplements in hypertension, 188b, 189t
Preauricular lymph nodes, 6f
Precordium, 7
Prediabetes, 364
Premature ventricular complexes, 173
Premenstrual dysphoric disorder, 261–262
Premenstrual syndrome, 261–262
Prenatal history, 27
Prostate cancer, 301–302
Prostate gland, benign hypertrophy of, 301
Prostatitis, 300–301
Proteinuria, 68
Prozac. See Fluoxetine
Psoas sign, 223–224
Psoriasis, 3f, 83–85
Psychiatric disorders, 424–440
akathisia, 435
anxiety disorders, 432–436, 434t
bipolar disorder, 432
cognitive impairment, 437–440, 437b
dementia, 438–440
depression, 425–431, 427t
dysthymic disorder, 425

692
 dystonias, 435
extrapyramidal symptoms, 435
generalized anxiety disorder, 433
history in, 424
initial office visit for, 424–425
laboratory test in, 425
mental status interview for, 424–425
panic disorder, 433–434
parkinsonism, 435
seasonal affective depressive disorder, 430–431
serotonin syndrome, 431–432
Psychosocial history, 2
Ptosis, ocular, 14t
Puberty, 31, 32–33b
Pubic hair, 32–33b
Pulmonary embolism, 163
Pulmonary function testing, 123, 124–125t, 125t
Pulse oximetry, 73–74, 123
Punch biopsy, 109
Pupil(s)
dilation of, 3
ophthalmologic examination of, 14t
reactivity testing of, 3
Pyelonephritis, acute, 291–293
Pyloric stenosis, 410
R
Rabies, 113–114
Radial pulse, 8f
Radiology, 75
Rales, 4
in elderly, 51b
Raynaud’s phenomenon, 196–197
Rectal examination, 9
Red blood cells, 67
Referred pain, 222
Reflex testing

693
 in adults, 17–18, 17t
in children, 45, 45t
Remeron. See Mirtazapine
Renal calculi, 294–295
Respiratory assessment
geriatric, 51, 53t
tests for, 123
Respiratory rate, 35t
Respiratory syncytial virus, 409
Respiratory system
focused examination of, 18–19
pediatric, 39–40
physical examination of, 4, 6f
Respiratory tract disorders
asthma, 126–131, 127–129t
in children, 400–407
chronic obstructive pulmonary disease, 51, 73, 132–133, 134t
community acquired pneumonia, 135–137
lower, in children, 407–410
pulmonary function testing for, 123, 124–125t, 125t
tests for assessing, 123
Restless leg syndrome, 350–351
Restrictive lung diseases, 123
Reticulocyte index, 210–211
Retinopathy, diabetic, 391
Review of systems
in adults, 2
in children, 30–33
Rheumatoid arthritis, 345
Rheumatoid factor, 74
Rhinitis, allergic, 150
Rhinosinusitis
acute bacterial, 404–405
in adults, 150–151
in children, 404–405
Rhonchi, 4

694
Rickettsial disease, 115
Rinne test, 3
Rocky Mountain spotted fever, 115
Romberg’s test, 17, 44
Rooting reflex, 45t
Rosacea, 1f, 89–90
Roseola, 97
Rotator cuff injuries, 326
Routine well-woman examination, 21
Rovsing’s sign, 223–224
S
Salmonella, acute diarrhea due to, 241–242
Sarcoptes scabiei, 120–121
Scabies, 120–121
Scarlet fever rash, 4f, 91
Schistocytes, 67
Scoliosis screening, 415–416
Scratches, 108
Seasonal affective depressive disorder, 430–431
Seborrheic dermatitis, 1f, 83
Secretagogues, 379–382t
Seizures, 308, 309f
findings in, 308b
syncope related to, 314
Selective serotonin reuptake inhibitors, 427t
for anxiety, 434t
withdrawal from, 430
Sensorineural hearing disorder, 3
Sensory testing, geriatric, 51, 52t, 59b
Serotonin syndrome, 431–432
Sexual abuse, 47
Sexual maturity, Tanner’s rating of, 31, 32–33b
Sexually transmitted diseases, 280–286
SGLT2 inhibitors, 382
Shigella, acute diarrhea due to, 242
Shingles, 99–100

695
Short Portable Mental Status Questionnaire, 60, 61b
Shoulder
anatomy of, 323f
range of motion in, 324, 325f
Shoulder pain, 322–327, 324t
referred, 324t
Sickle cell anemia, 218
Sinus bradycardia, 172–173
Sinus tachycardia, 170
Sinuses, 4
Sinusitis, 150–151
in children, 404–405
Skin cancer, 107–108
Skin disorders, 77–122
bite-and sting-related, 112–114
fungal, 101–103
infectious, 90–95
lesions, 105–108
pigmentation, 103–105
rosacea, 1f, 89–90
wound care, 108–111
Skin examination
in adults, 3
in children, 35–36
Skin tags, 105–106
Skull, 44
Sleep apnea, obstructive, 138–139, 139b
Sleep habits, 27
SMBG. See Blood glucose, self-monitoring of
Snake bites, 112
Social history, 30
Specific gravity, of urine, 69–70t
Speech disturbances, 12, 13t
Spermicides, 254
“Spherocytes,” 67
Spider bites, 116–117

696
Spine, upper, 322f
Spleen, 41
Sports physical examination, 21–24
Sprains, 342, 342t
Spurling’s maneuver, 321
Squamous cell carcinoma, 7f, 107
SSRIs. See Selective serotonin reuptake inhibitors
St. John’s wort, 429
Staphylococcus aureus, acute diarrhea due to, 241
Startle reflex, 38
Stasis dermatitis, 193–194
Statins, for hyperlipidemias, 175t
Stepping response reflex, 45t
Stereognosis, 17
Steroids
for atopic dermatitis, 77–79, 78t
for contact dermatitis, 80
oral, equivalencies for, 86t
topical, 78, 78t
dispensing, 85
types of, 78t
Sting injuries, 121–122
Strains, 342, 342t
Streptococcal scarlet fever, 4f
Stress incontinence, 295–296
Stridor, 4
Stye, 146
Submandibular lymph nodes, 6f
Submental lymph nodes, 6f
Sulfonylureas, 379
Superficial thrombophlebitis, 192
Supraclavicular lymph nodes, 6f
Suturing, 109–111, 110t
Syncope, 306–307
Syphilis, 283–284
Systolic murmurs, 156–157t

697
T
Tachycardia
paroxysmal supraventricular, 172
sinus, 170
Talipes equinovarus, 418
Tanner’s sexual maturity rating, 31, 32–33b
Tardive dyskinesia, 435–436
Teeth
aging changes in, 55t
dental chart of, 30, 31f
Tendinitis
of foot, 340
rotator cuff, 326
Tension headache, 315
Testicles, undescended, 413
Testicular cancer, 302–303
Testicular examination, 9
Testicular torsion, 302
Tetanus prophylaxis, 93t
Thalassemia, 217–218
Thoracic outlet syndrome, 326
Thrombocytopenia, 68
Thrombocytosis, 67–68
Thrombophlebitis, superficial, 192
Thyroid cancer, 361
Thyroid disorders, 359–361, 361t
Tick bites, 114–116
Timed “Up and Go” Test, 63
Tinea, 8f, 101–102
Tinea versicolor, 101
Tinel’s test, 328
Tinetti Balance and Gait Evaluation, 62–63t, 63–64
Tinnitus, 146–147
Tonic neck reflex, 45t
Tonsils, 4
Torticollis, 42

698
Total iron-binding capacity, 212
Total lung capacity, 123, 125t
Transient incontinence, 297, 298b
Travelers’ diarrhea, 244
Trazodone, 427t, 429
Tremor, 308–310
in Parkinson’s disease, 310
Trichomoniasis vaginitis, 281
Tricyclic antidepressants, 427t, 429
withdrawal from, 430
Trigeminal nerve, 15–16t, 44
Trochlear nerve, 15–16t, 44
Tuberculosis, 137–138
Two-point discrimination test, 17
Tympanic membrane
description of, 4f, 37
perforation of, 401
Tympanostomy tubes, acute otitis media with, 402
U
Ulcer(s)
differential diagnosis of, 192, 206–207
peptic, 230–231
Ulcerative colitis, 240–241
Ulcerative keratitis, 144
Ulnar pulse, 8f
Umbilicus, 4f, 41
Unna boot, 199–200
Urge incontinence, 296
Uric acid, 75
Urinary incontinence, 295–297
Urinary tract disorders, 287–304
bladder cancer, 293
chronic kidney disease, 298–300
epididymitis, 302
erectile dysfunction, 303–304
glomerulonephritis, 293

699
 incontinence, 295–297
interstitial cystitis, 288–290
kidney stones, 294–295
in men, 300–304
prostate cancer, 301–302
prostatitis, 300–301
pyelonephritis, 291–293
testicular cancer, 302–303
testicular torsion, 302
Urinary tract infection, 288, 414–415
Urine culture, 68
Urine tests, 68, 69–70t
Urticaria, 81–82
Uterus
abnormal bleeding from, 264–265
physical examination of, 10, 11f
positions of, 11f
V
Vagina
examination of, 10
wet prep examination of, 10, 12f
Vaginitis
atrophic, 278
bacterial, 277–278
trichomoniasis, 281
Vagus nerve, 15–16t, 44
Varicella, 100–101
Varicose veins, 194
Vascular/blood disorders, 191–219
anemia, 209–219
chronic peripheral vascular disease, 191–205
venous, arterial, and diabetic ulcers, 192, 206–207
wound care and treatment for, 209b
Vasovagal syncope, 306
Venlafaxine, 427t, 429
Venous insufficiency, chronic, 192–193

700
Venous ulcers, 206–207
Verruca vulgaris, 96–97
Vertigo, 305–308, 307–308b
Vesicular breath sounds, 6f
Visceral pain, 220, 354
Visual acuity
in adults, 3, 13, 13t
in children, 36
Vital signs
in adults, 2–3
in children, 35t
Vitamin B12, 216
Vitamin D deficiency, 73
Vitiligo, 105
Vulnerable Elders Survey, 62, 64–65t
Vulvar vestibulitis, 279–280
Vulvitis, 279
Vulvodynia, 277–278
Vulvovaginitis, 421–422
W
Warfarin therapy, 200–205, 201t, 204–205t
Warts, 5f, 96–97
genital, 285–286
Weber’s test, 3
Well-child visit, 25–26
Well-woman examination, routine, 21
Wernicke’s aphasia, 13t
West Nile virus, 117
Wet prep, vaginal, 10, 12f
Wheezes, 4
White blood cells, 66–67
Women, physical examination of. See Gynecologic assessment
Wound(s)
debridement of, 208
differentiation of, 206–208
stage 1, 208

701
 stage 2, 208
stage 3/4, 208
Wound care, 93t, 108–111, 110t
chronic, 205–209
vascular, 205–209
Wrist disorders, 329–331, 330t
X
Xerosis, 80–81
Y
Yesavage Geriatric Depression Scale, 61t

702
Inside back cover

Abbreviations

A1c Hemoglobin A1c

AAA Abdominal aortic aneurysm
Ab Abortion
ABG Arterial blood gas
ABI Ankle-brachial index
AC Acromioclavicular (joint)
ACE Angiotensin converting enzyme
ACR Albumin:creatinine ratio
ACS Acute coronary syndrome
ADH Antidiuretic hormone
ADHD Attention deficit hyperactivity disorder
ADL Activities of daily living
AGN Acute glomerulonephritis
ALS Amyotropic lateral sclerosis
ALT Alanine aminotransferase (transaminase)
AMI Acute myocardial infarction
ANA Antinuclear antibody
anti HBe Hepatitis B (e) antibody
anti HBs Hepatitis B antibody
AOM Acute otitis media
AP Anteroposterior
ARB Angiotensin receptor blocker
ASA Aspirin
ASC-US Atypical squamous cell of undetermined significance
ASCVD Arteriosclerotic cardiovascular disease
AST Aspartate aminotransferase (transaminase)
AUB Abnormal uterine bleeding
AV Atrioventricular
BV Bacterial vaginitis
BMD Bone mineral density
BMI Body mass index
BP Benzoyl peroxide
BPH Benign prostatic hypertrophy
BUN Blood urea nitrogen
BUS Bartholin’s –urethral-Skene’s (glands)
CAP Community acquired pneumonia
CABG Coronary artery bypass graft
CAD Coronary artery disease
CCB Calcium channel blocker
CDC Centers for Disease Control and Prevention
CF Cystic fibrosis

703
CFU Colony forming units
CHD Coronary heart disease
CIS Carcinoma in situ
CK Creatine kinase
CKD Chronic kidney disease
CML Chronic myelocytic leukemia
CMT Cervical motion tenderness
CMV Cytomegalovirus
CN Cranial nerve
COC Combined oral contraceptive
CP Cerebral palsy
CPAP Continuous positive airway pressure
CRF Chronic renal failure
CRP C-reactive protein
C&S Culture and sensitivity
CSF Cerebrospinal fluid
CT Computed tomography (x-ray examination)
CTA Clear to auscultation
CTS Carpal tunnel syndrome
CVA Cerebrovascular accident
CVAT Costovertebral angle tenderness
CVD Cardiovascular disease
DDAVP Synthetic vasopressin (posterior pituitary hormone)
DDP-4 Dipeptidyl peptidase (inhibitor – diabetes medication)
DI Diabetes insipidus
DIC Disseminated intravascular coagulation
DJD Degenerative joint disease
DKA Diabetic ketoacidosis
DM Diabetes mellitus
DOE Dyspnea on exertion
DP Dorsalis pedis (pulse)
DPI Dry powder inhaler
DTR Deep tendon reflex
DVT Deep venous thrombosis
EBV Epstein-Barr virus
EC/ECP Emergency contraception/emergency contraceptive pill
ECG Electrocardiogram (may also see as EKG)
EEG Electroencephalogram
eGFR Estimated glomerular filtration rate
EIA Exercise induced asthma
EMG Electromyogram
ENT Ear-nose-throat (physician specialist)
EOM Extraocular movement
EPS Extrapyramidal symptom
ESR Erythrocyte sedimentation rate
ETOH Alcohol (drinking)

704
FBG Fasting blood glucose
FEV1 Forced expiratory volume in 1 second
FMS Fibromyalgia syndrome
FOBT Fecal occult blood test
FSH Follicle-stimulating hormone
FVC Forced vital capacity
GAD Generalized anxiety disorder
GC/CT Gonococcus and chlamydia trachomatis
GGT Gamma-glutamyl transpeptidase
GI Gastrointestinal
GLP-1 Glucagon-like peptide (receptor agonist - diabetes medication)
GTT Glucose tolerance test
GU Genitourinary
H/A Headache
HAV Hepatitis A virus
HbcAg Hepatitis B core antigen
HBeAg Hepatitis B (e) antigen
HBsAg Hepatitis B surface antigen
HBV Hepatitis B virus
hCG Human chorionic gonadotropin
HCV Hepatitis C virus
HDL High-density lipoprotein
HF Heart failure
HIDA Hepatobiliary scan (x-ray examination)
HLA Human leukocyte antigen
HPF High-powered field
HPV Human papillomavirus
HRT Hormone replacement therapy
HSIL High-grade squamous intraepithelial lesion
HSV Herpes simplex virus
HTN Hypertension
I&D Incision and drainage
IBD Inflammatory bowel disease
IBS Irritable bowel syndrome
ICS Inhaled corticosteroid
IDA Iron deficiency anemia
Ig immunoglobulin
IGT Impaired glucose intolerance
INR International normalized ratio
IUD Intrauterine (contraceptive) device
IVP Intravenous pyelogram
JVD Jugular venous distention
KOH Potassium hydroxide
KUB Kidney-ureter-bladder (x-ray examination)
LA Left atrial
LABA Long-acting beta agonist

705
LAMA Long-acting muscarinic agonist
LBBB Left bundle branch block
LDH Lactate dehydrogenase
LDL Low-density lipoprotein
LES Lower esophageal sphincter
LFT Liver function test
LH Luteinizing hormone
LMP Last menstrual period
LOC Level of consciousness
LSB Left sternal border
LSIL Low-grade squamous intraepithelial lesion
LV Left ventricular
LVH Left ventricular hypertrophy
MCH Mean corpuscular hemoglobin
MCV Mean corpuscular volume
MDI Metered dose inhaler
MDR-TB Multi-drug-resistant tuberculosis
MI Myocardial infarction
MRSA Methicillin-resistant staphylococcus aureus
MS Multiple sclerosis
MVP Mitral valve prolapse
NAAT Urine test for gonorrhea and chlamydia
NAFLD Non-alcoholic fatty liver disease
NASH Non-alcoholic steatohepatitis
NSAID Non-steroidal anti-inflammatory drug
N/V Nausea and vomiting
NYHA New York Heart Association
O&P Ova and parasites
OA Osteoarthritis
OB Occult blood
OC Oral contraceptive
OCD Obsessive-compulsive disorder
OD Overdose
OE Otitis externa
OHA Oral hypoglycemic agent
OME Otitis media with effusion
OSA Obstructive sleep apnea
OTC Over-the-counter
PAD Peripheral arterial disease
PCOS Polycystic ovarian syndrome
PE Pulmonary embolism
PEF Peak expiratory flow
PFT Pulmonary function test
PHN Post-herpetic neuralgia
PID Pelvic inflammatory disease
PMI Point of maximal impulse

706
PMS Premenstrual syndrome
PND Paroxysmal nocturnal dyspnea
POA Power-of-attorney
POP Progestin only pill
PPI Proton pump inhibitor
PSA Prostate-specific antigen
PT Posterior tibialis (pulse)
PTCA Percutaneous transluminal coronary angioplasty
PTSD Posttraumatic stress disorder
PTT Partial thromboplastin time
PUD Peptic ulcer disease
PUVA Psoralen plus ultraviolet A (light therapy)
PVC Premature ventricular contraction
PVR Postvoid residual
RA Rheumatoid arthritis
RCA Right coronary artery
RF Rheumatoid factor
RLS Restless legs syndrome
ROM Range of motion
RPR Rapid plasma reagin (test for syphilis)
RSV Respiratory syncytial virus
SABA Short-acting beta agonist
SBE Subacute bacterial endocarditis
SCA Sickle cell anemia
SGLT2 Sodium-glucose-co-transporters (diabetes medication)
SIL Squamous intraepithelial lesion
SLE Systemic lupus erythematosus
SLR Straight leg raise
SNRI Selective norepinephrine reuptake inhibitors
SOB Shortness of breath
S/S Signs and symptoms
SSRI Selective serotonin reuptake inhibitor
STI Sexually transmitted infection
SVT Supraventricular tachycardia
T4 Thyroxine
TB Tuberculosis
TCA Tricyclic antidepressant
TIA Transient ischemic attack
TIBC Total iron-binding capacity
TMJ Temporomandibular joint
TMP-SMZ Trimethoprim-sulfamethoxazole (Bactrim)
TSH Thyroid-stimulating hormone
TTP Thrombotic thrombocytopenic purpura
UCG Urine chorionic gonadotropin (pregnancy test)
UGI Upper gastrointestinal (x-ray examination)
URI Upper respiratory (tract) infection

707
U/S Ultrasound
UTI Urinary tract infection
VDRL Venereal Disease Research Laboratories (test for syphilis)
VLDL Very-low-density lipoprotein
V/D Vomiting and diarrhea
VT Ventricular tachycardia
V/Q Ventilation perfusion (ratio)
WNL Within normal limits

708
Color Plates

COLOR PLATE 1. Papular and pustular acne (mild). Several papules are
localized on the cheeks. Source: (From Habif, T.P. [1996]. Clinical dermatology: A
color guide to diagnosis and therapy [3rd ed.]. St. Louis: Mosby.)

COLOR PLATE 2.The classic appearance of rosacea. Multiple papules

and a few pustules are scattered on the nose and cheeks. The nose
shows almost confluent erythema. Source: (From White, G.M., & Cox, N.H.
[2002]. Diseases of the skin: A color atlas and text. St. Louis: Mosby.)

709
 COLOR PLATE 3. Epidermal inclusion cyst. Source: (From White, G.M., & Cox,
N.H. [2002]. Diseases of the skin: A color atlas and text. St. Louis: Mosby.)

COLOR PLATE 4. Seborrheic dermatitis. Source: (Courtesy William D. James, MD.

From Habif, T.P. [1996]. Clinical dermatology: A color guide to diagnosis and therapy [3rd
ed.]. St. Louis: Mosby.)

710
 COLOR PLATE 5. Flexural atopic dermatitis with lichenification. Source:
(From White, G.M., & Cox, N.H. [2002]. Diseases of the skin: A color atlas and text. St. Louis:
Mosby.)

COLOR PLATE 6. Allergic contact dermatitis to Rhus. The classic

appearance of allergic contact dermatitis is illustrated in this patient who
came into contact with poison oak. The lesions are linear but not following
Blaschko’s lines. The eruption is microvesicular and extremely pruritic.
Source: (From White, G.M., & Cox, N.H. [2002]. Diseases of the skin: A color atlas and text.
St. Louis: Mosby.)

711
COLOR PLATE 7. Diaper dermatitis. Source: (From White, G.M., & Cox, N.H. [2002].
Diseases of the skin: A color atlas and text. St. Louis: Mosby.)

COLOR PLATE 8. Candida dermatitis. Source: (From White, G.M., & Cox, N.H.
[2002]. Diseases of the skin: A color atlas and text. St. Louis: Mosby.)

COLOR PLATE 9. Scaly papules behind the ear and on the scalp in

712
psoriasis. Source: (From Weston, W.L., Lane, A.T., & Morelli, J.G. [2002]. Color textbook
of pediatric dermatology [3rd ed.]. St. Louis: Mosby.)

COLOR PLATE 10. Psoriasis vulgaris. Source: (From Callen, J.P., Greer, K.E.,
Paller, A.S., & Swinyer, L.J. [2000]. Color atlas of dermatology [2nd ed.]. Philadelphia: W.B.
Saunders.)

COLOR PLATE 11. Impetigo. Honey-colored moist crust just above the
upper lip. Source: (From Weston, W.L., Lane, A.T., & Morelli, J.G. [2002]. Color textbook of
pediatric dermatology [3rd ed.]. St. Louis: Mosby.)

713
COLOR PLATE 12. Perforating folliculitis. Source: (From Callen, J.P., Greer, K.E.,
Paller, A.S., & Swinyer, L.J. [2000]. Color atlas of dermatology [2nd ed.]. Philadelphia: W.B.
Saunders.)

COLOR PLATE 13. Cellulitis following self-manipulation of acne

pustule. Source: (From Weston, W.L., Lane, A.T., & Morelli, J.G. [2002]. Color textbook of
pediatric dermatology [3rd ed.]. St. Louis: Mosby.)

714
 COLOR PLATE 14. Red, rough eruption of trunk and arm in
streptococcal scarlet fever. Source: (From Weston, W.L., Lane, A.T., & Morelli, J.G.
[2002]. Color textbook of pediatric dermatology [3rd ed.]. St. Louis: Mosby.)

COLOR PLATE 15. Molluscum contagiosum. Small papules with a central

umbilication. Source: (From Callen, J.P., Greer, K.E., Paller, A.S., & Swinyer, L.J. [2000].
Color atlas of dermatology [2nd ed.]. Philadelphia: W.B. Saunders.)

715
COLOR PLATE 16. Lesions about the umbilicus. The lower abdomen and
umbilicus are commonly affected by nondescript, excoriated lesions in
scabies. Source: (From White, G.M., & Cox, N.H. [2002]. Diseases of the skin: A color atlas
and text. St. Louis: Mosby.)

COLOR PLATE 17. Common warts on a child’s fingers. Source: (From

Weston, W.L., Lane, A.T., & Morelli, J.G. [2002]. Color textbook of pediatric dermatology [3rd
ed.]. St. Louis: Mosby.)

COLOR PLATE 18. Herpes simplex labialis-recurrent lesions. Source: (From

Callen, J.P., Greer, K.E., Paller, A.S., & Swinyer, L.J. [2000]. Color atlas of dermatology [2nd

716
 ed.]. Philadelphia: W.B. Saunders.)

COLOR PLATE 19. Herpes zoster. Source: (From Callen, J.P., Greer, K.E., Paller,
A.S., & Swinyer, L.J. [2000]. Color atlas of dermatology [2nd ed.]. Philadelphia: W.B.
Saunders.)

COLOR PLATE 20. Herpes genitalis, male. Source: (Courtesy of Michael O.

Murphy, MD. From White, G.M., & Cox, N.H. [2002]. Diseases of the skin: A color atlas and
text. St. Louis: Mosby.)

717
 COLOR PLATE 21. Hand-foot-and-mouth disease. Source: (From Callen, J.P.,
Greer, K.E., Paller, A.S., & Swinyer, L.J. [2000]. Color atlas of dermatology [2nd ed.].
Philadelphia: W.B. Saunders.)

COLOR PLATE 22. Erosion of the tongue in a child with hand-foot-and-

mouth syndrome. Source: (From Weston, W.L., Lane, A.T., & Morelli, J.G. [2002]. Color
textbook of pediatric dermatology [3rd ed.]. St. Louis: Mosby.)

718
 COLOR PLATE 23. Slapped-cheek appearance of a child with
parvovirus B19 infection (erythema infectiosum). Source: (From Weston,
W.L., Lane, A.T., & Morelli, J.G. [2002]. Color textbook of pediatric dermatology [3rd ed.]. St.
Louis: Mosby.)

COLOR PLATE 24. Lacy pink eruption over the palms in erythema
infectiosum. Source: (From Weston, W.L., Lane, A.T., & Morelli, J.G. [2002]. Color
textbook of pediatric dermatology [3rd ed.]. St. Louis: Mosby.)

719
COLOR PLATE 25. Multiple actinic keratosis. Source: (From Callen, J.P., Greer,
K.E., Paller, A.S., & Swinyer, L.J. [2000]. Color atlas of dermatology [2nd ed.]. Philadelphia:
W.B. Saunders.)

COLOR PLATE 26. Basal cell carcinoma of nodular type with ulceration
affecting the vulva. Source: (From White, G.M., & Cox, N.H. [2002]. Diseases of the
skin: A color atlas and text. St. Louis: Mosby.)

720
 COLOR PLATE 27. Squamous cell carcinoma. Malignant degeneration
occurred in an actinic keratosis that had been present for years. Source:
(From Habif, T.P. [1996]. Clinical dermatology: A color guide to diagnosis and therapy [3rd
ed.]. St. Louis: Mosby.)

COLOR PLATE 28. Malignant melanoma on the chest of an adolescent

male. Source: (From Weston, W.L., Lane, A.T., & Morelli, J.G. [2002]. Color textbook of
pediatric dermatology [3rd ed.]. St. Louis: Mosby.)

721
COLOR PLATE 29. Tinea cruris. Source: (From Callen, J.P., Greer, K.E., Paller, A.S.,
& Swinyer, L.J. [2000]. Color atlas of dermatology [2nd ed.]. Philadelphia: W.B. Saunders.)

COLOR PLATE 30. Tinea pedis as a result of Trichophyton rubrum.

Source: (From Callen, J.P., Greer, K.E., Paller, A.S., & Swinyer, L.J. [2000]. Color atlas of
dermatology [2nd ed.]. Philadelphia: W.B. Saunders.)

722
COLOR PLATE 31. Head lice. Numerous white nits attached to hairs. Source:
(From Weston, W.L., Lane, A.T., & Morelli, J.G. [2002]. Color textbook of pediatric
dermatology [3rd ed.]. St. Louis: Mosby.)

723